In-vivo and in-silico studies to identify toxicity mechanisms of permethrin with the toxicity-reducing role of ginger.

In this study, the toxic effects of permethrin on Allium cepa L. and the protective role of Zingiber officinale rhizome extract (Zoex) were investigated. In this context, 6 different groups were formed. While the control group was treated with tap water, the groups II and III were treated with 10 µg/mL and 20 µg/mL Zoex, respectively, and the group IV was treated with 100 µg/L permethrin. The protective effect of Zoex against permethrin toxicity was studied as a function of dose, and groups V and VI formed for this purpose were treated with 10 µg/mL Zoex + 100 µg/L permethrin and 20 µg/mL Zoex + 100 µg/L permethrin, respectively. After 72 h of germination, cytogenetic, biochemical, physiological, and anatomical changes in meristematic cells of A. cepa were studied. As a result, permethrin application decreased the mitotic index (MI) and increased the frequency of micronuclei (MN), and chromosomal abnormalities. The increase in malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) and the decrease in glutathione (GSH) indicate that permethrin causes oxidative damage. Compared to the control group, a 68.5% decrease in root elongation (p < 0.05) and an 81.8% decrease (p < 0.05) in weight gain were observed in the permethrin-treated group. It was found that the application of Zoex together with permethrin resulted in regression of all detected abnormalities, reduction in the incidence of anatomical damage, MN and chromosomal aberrations, and improvement in MI rates. The most significant improvement was observed in group VI treated with 20 µg/mL Zoex, and Zoex was also found to provide dose-dependent protection. The toxicity mechanism of permethrin was also elucidated by molecular docking and spectral studies. From the data obtained during the study, it was found that permethrin has toxic effects on A. cepa, a non-target organism, while Zoex plays a protective role by reducing these effects.

DNA fragmentation, chromosomal aberrations, and multi-toxic effects induced by nickel and the modulation of Ni-induced damage by pomegranate seed extract in Allium cepa L.

This study was designed to assess the recovery effect of pomegranate seed extract (PSEx) against nickel (Ni)-induced damage in Allium cepa. Except for the control group treated with tap water, five experimental groups were exposed to 265 mg L-1 PSEx, 530 mg L-1 PSEx, 1 mg L-1 NiCI2, 265 mg L-1 PSEx + 1 mg L-1 NiCI2, and 530 mg L-1 PSEx + 1 mg L-1 NiCI2, respectively. The toxicity of Ni was examined through the analysis of physiological (germination percentage, weight gain, and root length), cytotoxicity (mitotic index), genotoxicity (micronucleus, chromosomal anomalies, and Comet test), and biochemical (malondialdehyde, proline, chlorophyll a and chlorophyll b contents, the activities of superoxide dismutase and catalase) parameters. Meristematic cell defects were also investigated. The NiCl2-DNA interaction was evaluated through spectral shift analysis. Values of all physiological parameters, mitotic index scores, and chlorophyll contents decreased while micronucleus frequency, DNA tail percentage, chromosomal anomalies, proline, MDA, and enzyme activities increased following Ni administration. According to the tail DNA percentage scale, Ni application caused "high damage" to DNA. Ni-induced chromosomal anomalies were fragment, sticky chromosome, vagrant chromosome, bridge, unbalanced chromatin distribution, reverse polarization, and nucleus with bud. NiCl2-DNA interaction caused a hyperchromic shift in the UV/Vis spectrum of DNA by spectral profile analysis. Ni exposure impaired root meristems as evidenced by the formation of epidermis cell damage, flattened cell nucleus, thickened cortex cell wall, and blurry vascular tissue. Substantial recovery was seen in all parameters with the co-administration of PSEx and Ni. Recovery effects in the parameters were 18-51% and 41-84% in the 265 mg L-1 PSEx + 1 mg L-1 NiCI2 and 530 mg L-1 PSEx + 1 mg L-1 NiCI2 groups, respectively. The Comet scale showed that PSEx applied with Ni reduced DNA damage from "high" to "moderate." Ni-induced thickened cortex cell wall and blurry vascular tissue damage disappeared completely when 530 mg L-1 PSEx was mixed with Ni. PSEx successfully reduced the negative effects of Ni, which can be attributed to its content of antioxidants and bioactive ingredients.

Elucidating the toxicity mechanism of AFM2 and the protective role of quercetin in albino mice.

Aflatoxin M2 (AFM2) is a type of mycotoxin detected in milk or dairy products from animals consuming contaminated feed. In this study, the toxicity mechanism of AFM2 and the protective effects of quercetin were investigated in albino mice. For this purpose, the mice were divided into 6 groups and the groups were fed with quercetin and AFM2. The toxic effects of AFM2 and the protective properties of quercetin were investigated using physiological, biochemical and cytogenetic parameters. The genotoxic mechanism of AFM2 and the protective role of quercetin were investigated by molecular docking, which is an in silico model. As a result, 16 mg/kg b.w AFM2 administration caused serious changes in body weight, organ index, kidney and liver weight, and deterioration of antioxidant/oxidant balance in liver and kidney organs. The decrease in glutathione levels along with an increase in malondialdehyde (MDA) levels in the liver and kidney after AFM2 administration indicates that oxidative stress is induced. The increases in alanine transaminase (ALT) and aspartat transaminase (AST) levels, which are indicators of liver damage, and the increases in serum levels of blood urea nitrogen (BUN) and creatinine, which are indicators of kidney damage, confirm the damage in both organs. AFM2 also caused genotoxicity by inducing micronucleus (MN) and chromosomal abnormalities (CAs) in bone marrow tissue. It has been determined that AFM2, which exhibits genotoxicity as a result of its clastogenic and aneugenic effects, causes CAs by interacting with DNA. Quercetin provided significant protection by improving liver and kidney tissues, partial normalization in serum parameter levels, and severe reductions in MN and CAs. The highest protection was determined as 74.1% against dicentric chromosome formations in 50 mg/kg b.w quercetin application. The interaction of quercetin with xanthine oxidase and nitric oxide synthase enzymes was determined in silico with an inhibition constant in the range of 283.71-476.17 nM. These interactions cause changes in the activity of enzymes, reducing the oxidative load in the cell, and in this way, quercetin provides protection. All toxic effects induced by AFM2 were decreased with quercetin administration dose-dependently, and this protective effect was associated with quercetin's reduction of oxidative load by inhibiting the free radical-producing enzyme. All toxic effects caused by AFM2 were decreased with quercetin administration in a dose-dependent manner, and this protective effect was associated with quercetin's reduction of oxidative load by inhibiting the enzyme that produces free radicals.

GC-MS and HPLC supported phytochemical analysis of watercress and the protective role against paraben toxicity.

In this study, the phytochemical content of Nasturtium officinale R. Br. (watercress) leaf extract (Noex) and its protective effects against paraben toxicity were investigated. GC-MS and HPLC analyses were performed to determine the phytochemical content. Paraben toxicity and protective properties of Noex were investigated with the Allium test, and 6 different groups were formed for this purpose. Toxicity in each group was investigated by using physiological, cytogenetic, biochemical, and anatomical parameters. DNA-paraben interaction was investigated with spectroscopic analysis for the genotoxicity mechanism. As a result of the study, paraben (500 mM) caused a regression in the physiological parameters related to germination in Allium cepa L. bulbs. Paraben caused a 43.3% reduction in mitotic index (MI) rates compared to control, which is likely the reason for the decrease in germination-related parameters. With the application of paraben in root tip cells, the frequency of micronucleus (MN) and chromosomal aberrations (CAs) increased and a high genotoxic effect was observed. Paraben promoted CAs such as fragment, sticky chromosome, bridge, unequal distribution of chromatin, and irregular mitosis. It also caused anatomical damage in the form of epidermis cell damage, flattened cell nucleus, cortex cell damage, cortex cell walls thickening, and unclear vascular tissue in root tip meristem cells. Paraben-DNA interaction was caused by bathochromic and hypochromic shifts in the UV spectrum of DNA, indicating the intercalation mode of interaction. Paraben also caused an increase in malondialdehyde (MDA) levels, a decrease in glutathione (GSH) levels, and abnormalities in antioxidant enzyme levels (superoxide dismutase = SOD and catalase = CAT), thereby disrupting the antioxidant/oxidant dynamics in the cell. The basis of physiological, cytological, and genetic abnormalities was attributed to the oxidative stress in the cell. Administration of Noex produced a dose-dependent incremental improvement in paraben-induced abnormalities. The increase in GSH levels and the decrease in MDA levels observed as a result of the Noex application contributed to the restoration of antioxidant/oxidant balance, and this improvement was also reflected in other parameters. Application of 200 mg/L Noex provided a 24.2% improvement in the MI rate reduced by paraben, and accordingly, an increase in germination parameters was observed. Similarly, the frequencies of MN and CAs, which are signs of genotoxicity, decreased with the Noex application. As a result of the phytochemical analysis of Noex with HPLC and GC-MS, the presence of strong antioxidant and antimutagenic substances such as rutin, coumaric acid, ferrulic acid, L-serine, L-proline, and phytol were determined in Noex structure. The curative effects of Noex against paraben toxicity can be attributed to these active ingredients.

Qualitative and quantitative phytochemical screening of Nerium oleander L. extracts associated with toxicity profile.

In this study, phytochemical analysis and toxicity profile of leaf and flower extracts of Nerium oleander L. species collected from Giresun province (Turkey) were investigated. In phytochemical analyzes, the cardiac glycoside, alkaloid, saponin and tannin contents of the extracts were analyzed qualitatively and quantitatively. The physiological effects of extracts were determined by examining root elongation, weight gain and germination rates. Biochemical effects were determined by measuring the levels of malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT), which are indicators of oxidative stress. Cytotoxic and genotoxic effects were investigated by mitotic index (MI), micronucleus (MN) and chromosomal abnormality (CA) tests. N. oleander leaf and flower extract applications caused significant decreases in the physiological parameters of Allium bulbs. SOD and CAT activity in root tip cells increased significantly after the application of leaf extract compared to the control group. Similar changes were observed in the application of flower extract, but these increases were found to be at a lower level compared to the increases induced by the leaf extract. An increase in MDA levels and a decrease in GSH levels were observed in groups treated with leaf and flower extracts. These changes show that the extracts cause deterioration in antioxidant/oxidant balance. It was determined that the extracts, which caused a decrease in MI rates and an increase in MN and CAs frequencies, showed the most prominent cytotoxic and genotoxic effects at 250 µg/mL doses. These toxic effects were associated with the phytochemical content of the extracts, and it was thought that cardiac glycosides and alkaloids, whose presence were detected in qualitative and quantitative analyzes, may play an important role in toxicity. Studies investigating the therapeutic properties of plants as well as their toxic effects are insufficient, which leads to the fact that plants exhibiting potential toxicity are not well known. Therefore, this study will lead many studies on the toxicity profile of the phytochemical contents of plants. Therefore, this study will draw attention to the investigation of the toxicity profile and phytochemical contents of plants and will lead to similar studies.

Toxicity assessment of potassium bromate and the remedial role of grape seed extract.

In this study, the multiple toxic effects of potassium bromate were investigated in Allium cepa L., an indicator test material. In addition, the toxicity-reducing effects of grape seed extract (GSE) were tested. The toxicity was investigated by some physiological (germination percentage, root length, weight gain, relative injury rate), cytogenetic [mitotic index (MI), micronucleus (MN), and chromosomal abnormalities (CAs)], biochemical [malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) levels] and anatomical parameters. A. cepa bulbs were divided into 6 groups as control and five treatment groups (Group II: 465 mg/L GSE, Group III: 930 mg/L GSE, Group IV: 100 mg/L potassium bromate, Group V: 100 mg/L potassium bromate + 465 mg/L GSE, Group VI: 100 mg /L potassium bromate + 930 mg/L GSE). The bulbs were germinated for 72 h and at the end of the period the bulbs were subjected to routine preparations and made ready for analysis and measurements. As a result, potassium bromate exposure caused statistically significant (p < 0.05) decreases in all physiological parameter values. Potassium bromate application decreased MI by 41.6%, and increased the MN and CAs frequencies. CAs such as fragment, sticky chromosome, and vagrant chromosome, unequal distribution of chromatin, reverse polarization, nuclear bud and disordered mitosis were induced in root meristem cells. The mechanism of potassium bromate genotoxicity has been associated with DNA-potassium bromate interaction supported by spectral shift. Potassium bromate caused a decrease in GSH levels and an increase in MDA, SOD and CAT levels, thereby disrupting the antioxidant/oxidant balance in root tip cells. GSE administration in two different doses together with potassium bromate reduced the toxic effects and caused improvements in all parameters examined. The most significant reduction in toxicity was in group VI, which received 930 mg/L GSE, and there was an improvement about 18% in MI levels and an improvement about 44% in GSH levels in this group. While GSE application increased physiological parameters and GSH levels, it decreased MDA, SOD, CAT levels, MN and CAs frequencies. As a result, it has been determined that potassium bromate causes multi-directional toxicity at high doses and A. cepa is a very reliable indicator in determining this toxicity. In addition, GSE extract has been found to have a strong role in reducing the toxicity induced by potassium bromate.

Risk assessment of oxidative stress and multiple toxicity induced by Etoxazole.

Etoxazole is among the systemic pesticides with acaricidal and insecticidal characteristics. This paper reports the first evaluation of the toxic effects of Etoxazole on Allium cepa L. Etoxazole solutions were applied to three groups formed from A. cepa bulbs at 0.125 mL/L, 0.25 mL/L and 0.5 mL/L doses, respectively. The control group was treated with tap water throughout the experimental period. The toxic effects of Etoxazole became more apparent as the dose of Etoxazole was increased. The growth-limiting effect was most pronounced in the highest dose group with approximately 29%, 70% and 58.5% reductions in germination percentage, root elongation and weight gain, respectively. The genotoxic effect of Etoxazole was most severe in the 0.5 mL/L dose group. In this group, the mitotic index decreased by 30% compared to the control group, while the micronucleus frequency increased to 45.3 ± 3.74. The most observed aberrations were fragment, vagrant chromosome, sticky chromosome, unequal distribution of chromatin, bridge, reverse polarization and nucleus with vacuoles. The malondialdehyde level showed a gradual increase with increasing Etoxazole doses and reached 2.7 times that of the control group in the 0.5 mL/L Etoxazole applied group. Catalase and Superoxide dismutase activities increased in the groups exposed to 0.125 mL/L and 0.25 mL/L Etoxazole with dose dependence and decreased abruptly in the group treated with 0.5 mL/L Etoxazole. Etoxazole triggered meristematic cell damages, such as epidermis cell damage, thickening of cortex cell walls, flattened cell nucleus and indistinct transmission tissue. Considering the versatile toxicity induced by Etoxazole, we announce that this chemical has the potential to cause serious damage to non-target organisms. It should be noted that the higher the dose of exposure, the more severe the level of damage. This study will be an important reminder to limit the indiscriminate use of this highly risky agrochemical.

Dose-dependent toxicity profile and genotoxicity mechanism of lithium carbonate.

The increasing widespread use of lithium, which is preferred as an energy source in batteries produced for electric vehicles and in many electronic vehicles such as computers and mobile phones, has made it an important environmental pollutant. In this study, the toxicity profile of lithium carbonate (Li2CO3) was investigated with the Allium test, which is a bio-indicator test. Dose-related toxic effects were investigated using Li2CO3 at doses of 25 mg/L, 50 mg/L, and 100 mg/L. The toxicity profile was determined by examining physiological, cytotoxic, genotoxic, biochemical and anatomical effects. Physiological effects of Li2CO3 were determined by root length, injury rate, germination percentage and weight gain while cytotoxic effects were determined by mitotic index (MI) ratio and genotoxic effects were determined by micronucleus (MN) and chromosomal aberrations (CAs). The effect of Li2CO3 on antioxidant and oxidant dynamics was determined by examining glutathione (GSH), malondialdehyde (MDA), catalase (CAT) and superoxide dismutase (SOD) levels, and anatomical changes were investigated in the sections of root meristematic tissues. As a result, Li2CO3 exhibited a dose-dependent regression in germination-related parameters. This regression is directly related to the MI and 100 mg/L Li2CO3 reduced MI by 38% compared to the control group. MN and CAs were observed at high rates in the groups treated with Li2CO3. Fragments were found with the highest rate among CAs. Other damages were bridge, unequal distribution of chromatin, sticky chromosome, vagrant chromosome, irregular mitosis, reverse polarization and multipolar anaphase. The genotoxic effects were associated with Li2CO3-DNA interactions determined by molecular docking. The toxic effects of Li2CO3 are directly related to the deterioration of the antioxidant/oxidant balance in the cells. While MDA, an indicator of lipid peroxidation, increased by 59.1% in the group administered 100 mg/L Li2CO3, GSH, which has an important role in cell defense, decreased by 60.8%. Significant changes were also detected in the activities of SOD and CAT, two important enzymes in antioxidant defense, compared to the control. These toxic effects, which developed in the cells belonging to the lithium-treated groups, were also reflected in the tissue anatomy, and anatomical changes such as epidermis cell damage, cortex cell damage, flattened cell nucleus, thickening of the cortex cell wall and unclear vascular tissue were observed in the anatomical sections. The frequency of these changes also increased depending on the Li2CO3 dose. As a result, Li2CO3, which is one of the lithium compounds, and has become an important contaminant in the environment with increasing technological developments, caused a combined and versatile toxicity in Allium cepa L. meristematic cells, especially by causing deterioration in antioxidant/oxidant dynamics.

Turmeric (Curcuma longa L.) tends to reduce the toxic effects of nickel (II) chloride in Allium cepa L. roots.

The immense protection potential of plant-derived products against heavy metal toxicity has become a considerable field of research. The goal of the present study was to evaluate the mitigative ability of turmeric against nickel (II) chloride (NiCl2)-related toxicity in the roots of Allium cepa L. For this purpose, one control (treated with tap water) and five treatment groups (treated with 440 mg/L turmeric, 880 mg/L turmeric, 1 mg/L NiCI2, 1 mg/L NiCI2 + 440 mg/L turmeric, and 1 mg/L NiCI2 + 880 mg/L turmeric, respectively) of Allium bulbs were established. Experimental conditions were maintained at room temperature for 3 days. Physiological, biochemical, cytogenetic, and meristematic integrity parameters were analyzed in all groups. NiCl2 reduced germination percentage, root elongation, and weight gain. Following NiCl2 application, the frequency of aberrant chromosomes and micronuclei increased, while mitotic index decreased. NiCl2 caused an increase in oxidative stress, which was evident by increased malondialdehyde level and catalytic activities of superoxide dismutase and catalase. Epidermal and cortex cell injuries as well as deformed cell nuclei and indistinct transmission tissue were observed as a result of NiCl2 treatment. When applied alone, turmeric, which did not cause any negative effects, led to an improvement in all parameters depending on the dose when applied together with NiCl2. Data from the study suggests that turmeric has remarkable protection potential against NiCl2 in Allium cepa.

Paraquat toxicity in different cell types of Swiss albino mice.

In this study, toxicity caused by 50, 100 and 200 mg/kg b.w doses of Paraquat herbicide in Swiss albino mice was investigated. Body weight, liver and kidney organ weights, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) enzyme activities, blood urea nitrogen (BUN) and creatinine levels, malondialdehyde (MDA) and glutathione (GSH) levels in liver and kidney, micronucleus (MN) formation in buccal mucosal epithelium, erythrocyte and leukocyte cells and chromosomal aberrations (CAs) in bone marrow cells, viability of liver and kidney cells were investigated. Four groups were randomly formed from male Swiss albino mice (one control and three treatment groups). The control group mice were provided tap water and the mice in the treatment groups were treated orally with three different doses of Paraquat (50, 100 and 200 mg/kg b.w) in the drinking water for 28 days. At the end of the application, all mice were sacrificed and routine preparation procedures were carried out to examine physiological, biochemical, oxidative stress and genetic parameters. Paraquat administration decreased physiological parameters (body, liver and kidney organ weights), and increased biochemical parameters (AST, ALT, BUN, creatinine and MDA). GSH levels were decreased depending on the dose. Kidney and liver damage were confirmed by the trypan blue test. Paraquat administration promoted MN formation in buccal mucosal epithelium, erythrocyte and leukocyte cells depending on the dose. The highest MN frequency was observed in leukocyte cells exposed to a dose of 200 mg/kg b.w of Paraquat. Deteriorations in DNA integrity as a result of MN formations were supported by the comet assay. In addition, Paraquat promoted CAs such as break, fragment, acentric, dicentric, gap and ring in bone marrow cells. Break damage was the most common among these damages. These observed genotoxic effects occured as a result of the interaction of DNA and DNA-related proteins with Paraquat. Molecular docking studies showed that Paraquat binds to histone H4 protein with high affinity and has a high intercalation potential. As a result, Paraquat herbicide caused a significant toxicity by changing physiological, biochemical, oxidative stress and genetic parameters of Swiss albino mice depending on the application dose.

Comparative investigation of toxicity induced by UV-A and UV-C radiation using Allium test.

Organisms are increasingly exposed to ultraviolet (UV) rays of sunlight, due to the thinning of the ozone layer and its widespread use in sterilization processes, especially against the SARS-CoV-2 virus. The present study was conducted with the purpose of evaluating the damages of UV-A and UV-C radiations in Allium cepa L. roots. The effects of two different types of UV on some physiological, biochemical, cytogenotoxic, and anatomical parameters were investigated in a multifaceted study. Three groups were formed from Allium bulbs, one of which was the control group. One of the other groups was exposed to 254 nm (UV-C) and the other to 365 nm (UV-A) UV. Growth retardation effect of UV was investigated with respect to germination percentage, total weight gain, and root elongation, while cytogenotoxicity arisen from UV exposure was analyzed using mitotic index (MI) and chromosomal aberration (CA) and micronucleus (MN) frequency. Oxidative stress due to UV application was investigated based on the accumulation of malondialdehyde (MDA) and the total activities of superoxide dismutase (SOD) and catalase (CAT) enzymes. Also, anatomical changes induced by UV-A and UV-C were analyzed in root meristematic cells. UV treatments caused significant reductions in growth-related parameters. Both UV treatments caused a significant increase in MDA levels and induction of SOD and CAT enzymes in root meristematic cells. A decrease in MI and an increase in the frequency of MN and CAs were observed in root tip cells, indicating the cytogenotoxic effect of UV application. Anatomical damages such as epidermis cell damage, cortex cell damage, necrotic zones, giant cell nucleus, and indistinct transmission tissue occurred in cells exposed to UV. All of the physiological, biochemical, cytogenetic, and anatomical damages observed in this study were more severe in cells treated with UV-C compared to UV-A. This study suggested that UV exposure triggered growth inhibition, cytogenotoxicity, oxidative stress, and meristematic cell damages in A. cepa roots depending on the wavelength.

Multi-protective role of Echinacea purpurea L. water extract in Allium cepa L. against mercury(II) chloride.

Mercury (Hg) is a persistent and dangerous heavy metal with genotoxic properties. Echinacea purpurea L. is a well-known therapeutic plant with anti-inflammatory, antioxidant, and anti-tumor properties. In this study, multi-protective role of Echinacea purpurea L. extract against toxicity caused by mercury(II) chloride (HgCI2) on Allium cepa L. investigated in a multifaceted way. As a consequence of 100 mgL-1 HgCI2 administration, root elongation, weight increase, germination rate, and mitotic index were reduced, whereas micronucleus frequency, chromosomal abnormalities frequency, meristematic cell injuries severity, malondialdehyde level, catalase, and superoxide dismutase activity were increased. On the other hand, co-administration of increasing doses of E. purpurea extract (265 mgL-1 and 530 mgL-1) and HgCI2 gradually alleviated all observed toxic effects of HgCI2. Protective role of E. purpurea extract against HgCI2-toxicity on A. cepa were clearly demonstrated in this study. The results of this study will lead to future researches investigating use of E. purpurea extract against genotoxic contaminants.

Extenuating role of lycopene against 254-nm UV-C radiation-mediated damages in Allium cepa L. roots.

UV-C exposure has become a crucial risk for living organisms due to its widespread use in sterilization. In this study, the mitigating potential of lycopene was investigated against UV-C-mediated toxicity in Allium cepa L. roots. Allium bulbs were separated into six groups which treated with tap water, 215 mg/L lycopene, 430 mg/L lycopene, 254-nm UV radiation, 215 mg/L lycopene + 254-nm UV radiation, and 430 mg/L lycopene + 254-nm UV radiation. Germination percentage, root length, weight gain, mitotic index, micronucleus frequency, and other chromosomal aberrations as well as meristematic cell damages were investigated in all groups. Malondialdehyde level and the activities of superoxide dismutase and catalase enzymes were also analyzed to understand the severity of oxidative stress. UV-C radiation was revealed to negatively affect all parameters investigated, while the mitigating activities of lycopene against UV-C-mediated toxicity were dose-dependent. Therefore, the study evidently demonstrated the promising potential of lycopene in the protection against the detrimental effects of UV-C exposure in A. cepa.

The Potential Risk Assessment of Phenoxyethanol with a Versatile Model System.

In this study, the toxic effects of phenoxyethanol (Phy-Et), which is widely used in cosmetic industry, has been investigated with Allium test by means of physiological, cytogenetic, anatomical and biochemical parameters. To determine the changes in physiological reactions weight gain, relative injury rate, germination percentage and root length were investigated. Malondialdehyde, superoxide dismutase, glutathion and catalase levels were analyzed as biochemical parameters for determining the presence of oxidative stress. Mitotic index, micronucleus and chromosomal abnormality frequencies were studied as cytogenetic evaluation and the anatomical changes in root tip cells were investigated by cross sections. Changes in surface polarity and wettability were investigated by taking contact angle measurements of pressed root preparations. The mechanism of toxicity has been tried to be explained by these contact angles and this is the first study using contact angle measurements in toxicity tests. Consequently, exposure to Phy-Et resulted in a decrease in all measured physiological parameters and in mitotic index. In contrast, significant increases in the micronucleus and chromosomal abnormality frequencies were observed and the most significant toxic effect was found in 10 mM Phy-Et treated group. Phy-Et application induced oxidative damage and caused a significant increase in malondialdehyde level and a decrease in glutathione level compared to control group. Also a response occured against oxidative damage in superoxide dismutase and catalase activity and the activities increased in 2.5 mM and 5 mM Phy-Et treated groups and decreased in 10 mM Phy-Et treated groups. Furthermore, Phy-Et treatment resulted in some anatomical damages and changes such as necrosis, cell deformation and thickening of the cortex cell wall in root tip meristem cells of A. cepa. In the contact angle measurements taken against water, it was found that the wettability and hydrophilicity of the root preparations treated with Phy-Et were reduced, and this was the explanation of the growth abnormalities associated with water uptake. As a result, it was found that Phy-Et application caused toxic effects on many viability parameters and A. cepa test material was a reliable biomarker in determining these effects.

Aneugenic, clastogenic, and multi-toxic effects of diethyl phthalate exposure.

Diethyl phthalate (DEP) is a compound which is used in many industrial fields, especially in cosmetic sector and causes contamination in air, water, and soil due to its widespread usage. In this study, the potential toxic effects of DEP were investigated by using physiological, anatomical, biochemical, and cytogenetic parameters in Allium cepa. The micronucleus (MN) test specifically aimed to elucidate the aneugenic and clastogenic effects of DEP. Physiological effects were determined by germination percentage, root length, weight gain parameters, and cytogenetic effects were investigated by mitotic index (MI) and chromosomal abnormality (CA) test. Malondialdehyde (MDA) level, catalase (CAT), and superoxide dismutase (SOD) activities were investigated as oxidative damage indicators and structural changes were investigated with anatomical cross sections. For this purpose, Allium cepa bulbs were divided into four groups as control and application groups and the application groups were germinated with 1.0, 2.2, and 4.4 µM DEP for 72 h. As a result, it was determined that germination percentage, weight gain and root length decreased, CA frequency, MDA level, SOD, and CAT activities were increased in DEP-treated groups when compared with the control group. DEP has been found to induce CA in root tip cells such as fragment, chromosome bridge, c-mitosis, sticky chromosome, and unequal chromatin distribution. When MN formations induced by DEP application were examined, both large-scale and small-scale MNs were determined. MN formation in both sizes indicates that DEP has both clastogenic and aneugenic effects. And also, it was found that DEP application caused structural changes and especially anatomic damages such as necrosis in 4.4 µM DEP application. As a result, it was found that DEP caused various toxic effects depending on the dose and that A. cepa test material was a useful indicator in determining these effects.

Protective Effects of ß-Carotene Against Ammonium Sulfate Toxicity: Biochemical and Histopathological Approach in Mice Model.

In this study, the protective role of ß-carotene against ammonium sulfate-induced toxicity has been evaluated in Mus musculus var. albino mice, along with biochemical and histopathological parameters. Some biochemical parameters such as aspartate transaminase (AST), alanine transaminase (ALT), blood urea nitrogen (BUN), creatinine and oxidative stress parameters, malondialdehyde (MDA), and glutathione (GSH) levels in kidney and liver tissues were investigated. The mice were randomly divided into six groups. Group I received intraperitoneal injections of 0.9% NaCl; group II received orally administered 250 mg kg-1 bw ß-carotene, group III received orally administered 500 mg kg-1 bw ß-carotene; group IV received 320 mg kg-1 bw ammonium sulfate; group V was given 250 mg kg-1 bw ß-carotene +320 mg kg-1 of bw ammonium sulfate; and group VI received orally administered 500 mg kg-1 of bw ß-carotene +320 mg kg-1 of bw ammonium sulfate. As a result, it was determined that the ammonium sulfate treatment causes significant changes in the biochemical and oxidative stress parameters and also in histological examinations. In group IV, significant increases in ALT, AST, BUN, MDA, and creatinine levels, and a significant decrease in GSH levels were observed compared with control group. In histopathological examinations, different pathological findings such as proteinaceous deposits, thickening of basement membrane, hyaline cast in kidney tissue and stellate cell, karyomegaly, and binucleated cells in liver tissue were observed. ß-carotene treatment in group V and VI ameliorated the elevated levels of liver enzymes and improved oxidative stress and histopathological findings, and so, it could be concluded that ß-carotene offered remarkable protection against ammonium sulfate-induced toxicity.

Protective effect of Ginkgo biloba L. leaf extract against glyphosate toxicity in Swiss albino mice.

The aim of the present study was to investigate the protective role of Ginkgo biloba L. leaf extract against the active agent of Roundup® herbicide (Monsanto, Creve Coeur, MO, USA). The Swiss Albino mice were randomly divided into six groups, with each group consisting of six animals: Group I (control) received an intraperitoneal injection of dimethyl sulfoxide (0.2 mL, once only), Group II received glyphosate at a dose of 50 mg/kg of body weight, Group III received G. biloba at a dose of 50 mg/kg of body weight, Group IV received G. biloba at a dose of 150 mg/kg of body weight, Group V received G. biloba (50 mg/kg of body weight) and glyphosate (50 mg/kg of body weight), and Group VI received G. biloba (150 mg/kg of body weight) and glyphosate (50 mg/kg of body weight). The single dose of glyphosate was given intraperitoneally. Animals from all the groups were sacrificed at the end of 72 hours, and their blood, bone marrow, and liver and kidney tissues were analyzed for aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), creatinine, malondialdehyde (MDA), and glutathione (GSH) levels and the presence of micronucleus (MN), chromosomal aberrations (CAs), and pathological damages. The results indicated that serum AST, ALT, BUN, and creatinine levels significantly increased in mice treated with glyphosate alone compared with the other groups (P<.05). Besides, glyphosate-induced oxidative damage caused a significant decrease in GSH levels and a significant increase in MDA levels of the liver and kidney tissues. Moreover, glyphosate alone-treated mice presented higher frequencies of CAs, MNs, and abnormal metaphases compared with the controls (P<.05). These mice also displayed a lower mean mitotic index than the controls (P<.05). Treatment with G. biloba produced amelioration in indices of hepatotoxicity, nephrotoxicity, lipid peroxidation, and genotoxicity relative to Group II. Each dose of G. biloba provided significant protection against glyphosate-induced toxicity, and the strongest effect was observed at a dose of 150 mg/kg of body weight. Thus, in vivo results showed that G. biloba extract is a potent protector against glyphosate-induced toxicity, and its protective role is dose-dependent.

The protective effect of royal jelly on chronic lambda-cyhalothrin toxicity: serum biochemical parameters, lipid peroxidation, and genotoxic and histopathological alterations in swiss albino mice.

The present study was undertaken to investigate the protective effect of royal jelly (RJ) against toxicity induced by a synthetic pyrethroid insecticide, lambda-cyhalothrin (LCT), in Swiss albino mice. Animals were randomly divided into six groups of six animals each. The control group received distilled water alone, whereas mice in the treatment groups received RJ alone (100 or 250 mg/kg of body weight), LCT alone (668 ppm), or RJ+LCT for 21 days. All mice (100%) survived until the end of experiment and were sacrificed at the end of 24 hours. Blood, bone marrow, and liver and kidney tissues were analyzed for aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), creatinine, malondialdehyde (MDA), and reduced glutathione (GSH) levels and micronucleus (MN) frequency, chromosomal aberrations (CAs), and pathological damages. Serum AST, ALT, BUN, and creatinine levels were elevated in mice treated with LCT alone compared with the other tested groups (P<.05). LCT-induced oxidative damage caused a significant decrease in GSH levels and a significant rise in MDA levels of liver and kidney tissues. LCT alone-treated mice presented higher frequencies (P<.05) of MNs, CAs, and abnormal metaphases compared with the controls; moreover, the mitotic index was lower than in controls (P<.05). Oral treatment with RJ significantly ameliorated the indices of hepatotoxicity, nephrotoxicity, lipid peroxidation, and genotoxicity induced by LCT. Both doses of RJ tested provided significant protection against LCT-induced toxicity, and its strongest effect was observed at the dose level of 250 mg/kg of body weight. In vivo results suggest that RJ is a potent antioxidant against LCT-induced toxicity, and its protective effect is dose dependent.

Protective role of grape seed extract against doxorubicin-induced cardiotoxicity and genotoxicity in albino mice.

In this study, the protective role of grape seed extract (GSE) against doxorubicin (DOX)-induced cardiotoxicity and genotoxicity has been evaluated in male Mus musculus var. albino mice. The micronucleus (MN) test in erythrocytes and the chromosome aberration (CA) test in bone marrow cells were used. Also, levels of reduced glutathione (GSH) and lipid peroxidation as malondialdehyde (MDA) in heart homogenates were measured, and in addition the changes in heart histology were investigated. The mice were randomly divided into six groups. Group I (negative control) received intraperitoneal injections of isotonic saline (0.02 mL/g) for 6 consecutive days, Group II received intraperitoneal injections of DOX (2.5 mg/kg of body weight, six doses every other day; cumulative dosage, 15 mg/kg of body weight) for 6 consecutive days, Group III received GSE (50 mg/kg of body weight, 21 doses every other day; cumulative dosage, 1,050 mg/kg of body weight) for 21 consecutive days, Group IV received GSE (150 mg/kg of body weight, 21 doses every other day; cumulative dosage, 3,150 mg/kg of body weight) for 21 consecutive days, Group V received GSE (50 mg/kg of body weight, 28 doses every other day; cumulative dosage, 1,400 mg/kg of body weight) for 28 consecutive days plus DOX (2.5 mg/kg of body weight, six doses every other day; cumulative dosage, 15 mg/kg of body weight) for 6 consecutive days, and Group VI received GSE (150 mg/kg of body weight, 28 doses every other day; cumulative dosage, 4,200 mg/kg of body weight) for 28 consecutive days plus DOX (2.5 mg/kg of body weight, six doses every other day; cumulative dosage, 15 mg/kg of body weight) for 6 consecutive days. DOX induced heart damage as indicated from a pronounced change in heart histology. In the DOX-treated group, there was a significant increase in MDA content in the heart homogenate, and the level of GSH was significantly decreased. DOX induced genotoxicity by increasing the number of aberrant metaphases (AMNs), MNs, and structural chromosomal aberrations (CAs) such as chromatid breaks, dicentrics, acentric fragments, and gaps and showed a detractive effect on the mitotic index (MI) of cells. Pretreatment with GSE before treatment with DOX significantly protected the heart tissue by ameliorating its antioxidant activity. In Groups V and VI, the MDA level of heart tissue was significantly decreased, and the GSH level was increased compared to the DOX-treated group. Moreover, GSE significantly protected bone marrow chromosomes from DOX-induced genotoxicity by reducing the total AMNs and the frequency of structural CAs. GSE treatment also decreased the frequency of MNs and increased the MI values. It could be concluded that GSE acts as a potent antioxidant to prevent heart damage and genotoxicity of bone marrow cells.

Protective role of Ginkgo biloba against hepatotoxicity and nephrotoxicity in uranium-treated mice.

The aim of the present study was to investigate the protective role of Ginkgo biloba leaf extract against uranium (U)-induced toxicity in Swiss albino mice. The mice were randomly divided into six groups, each consisting of six animals: Group I (control) received tap water alone, Group II received U at a dose of 5 mg/kg of body weight, Group III received G. biloba at a dose of 50 mg/kg of body weight, Group IV received G. biloba at a dose of 150 mg/kg of body weight, Group V received G. biloba (50 mg/kg of body weight) and U (5 mg/kg of body weight), and Group VI received G. biloba (150 mg/kg of body weight) and U (5 mg/kg of body weight) by oral gavage for 5 days. Serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), and creatinine levels were determined to assess liver and kidney function, respectively. Also, liver and kidney samples were taken for the determination of tissue malondialdehyde (MDA) and reduced glutathione (GSH) levels, and histopathological changes in liver and kidneys were investigated. The results indicated that there was a significant increase (P < .05) in selected serum parameters. Serum AST, ALT, BUN, and creatinine levels significantly increased in mice treated with U alone when compared to the other groups. Moreover, U-induced oxidative damage caused a significant decrease in GSH levels and a significant increase in MDA levels of liver and kidney tissues. Treatment with G. biloba produced amelioration in biochemical indices of hepatotoxicity and nephrotoxicity according to Group II. Each dose of G. biloba provided significant protection against U-induced toxicity, and its strongest effect was observed at a dose of 150 mg/kg of body weight. In vivo results showed that G. biloba extract is a potent protector against U-induced toxicity, and its protective role is dose-dependent.