Investigation of protective effect of resveratrol and coenzyme Q10 against cyclophosphamide-induced lipid peroxidation, oxidative stress and DNA damage in rats.

It is seen that cyclophosphamide, which is used in treating many diseases, especially cancer, causes toxicity in studies, and its metabolites induce oxidative stress. This study aimed to investigate the protective effects of resveratrol and Coenzyme Q10, known for their antioxidant properties, separately and together, against oxidative stress induced by cyclophosphamide. In this study, 35 Wistar albino male rats were divided into five groups. Groups; Control group, cyclophosphamide (CP) group (CP as 75 mg kg i.p. on day 14), coenzyme Q10 (CoQ10) + CP group (20 mg/kg i.p. CoQ10 + 75 mg kg i.p. CP), resveratrol (Res) + CP group (20 mg/kg i.p. Res + 75 mg/kg i.p. CP), CoQ10 + Res + CP group (20 mg/kg i.p Res + 20 mg/kg i.p CoQ10 and 75 mg/kg i.p.CP). At the end of the experiment, the cholesterol, creatinine and urea levels of the group given CP increased, while a decrease was observed in the groups given Res and CoQ10. Malondialdehyde level was high, glutathione level, superoxide dismutase and catalase activities were decreased in the blood and all tissues (liver, kidney, brain, heart and testis) of the CP given group. DNA damage and histopathological changes were also observed. In contrast, Res and CoQ10, both separately and together, reversed the CP-induced altered level and enzyme activities and ameliorated DNA damage and histopathological changes. In this study, the effects of Res and CoQ10 against CP toxicity were examined both separately and together.

Investigation of the efficacy of epidermal growth factor, boric acid and their combination in cartilage injury in rats: An experimental study.

OBJECTIVES: In this study, we aimed to determine the bioefficacy of epidermal growth factor (EGF), boric acid (BA), and their combination on cartilage injury in rats. MATERIALS AND METHODS: In in vitro setting, the cytotoxic effects of BA, EGF, and their combinations using mouse fibroblast cell (L929), human bone osteosarcoma cell (Saos-2), and human adipose derived mesenchymal stem cells (hAD-MSCs) were determined by applying MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] test. In in vivo setting, 72 rats were randomly divided into four groups. A standard chondral defect was created and microfracture was performed in all groups. Group A was determined as the control group. In addition to the standard procedure, Group B received 100 ng/mL of EGF, Group C received a combination of 100 ng/mL of EGF and 10 µg/mL of BA combination, and Group D 20 µg/mL of BA. RESULTS: The cytotoxic effect of the combinations of EGF dilutions (1, 5, 10, 25, 50, 100, 200 ng/mL) with BA (100, 300, 500 µg/mL) was observed only in the 72-h application period and in Saos-2. The cytotoxic effect of BA was reduced when combined with EGF. There was no significant difference in the histopathological scores among the groups (p=0.13). CONCLUSION: Our study showed that EGF and low-dose BA application had a positive effect on cartilage healing in rats. Significant decreases in recovery scores were observed in the other groups. The combination of EGF and BA promoted osteoblast growth. Detection of lytic lesions in the group treated with 20 µg/mL of BA indicates that BA may have a cytotoxic effect.

Synergistic toxicity of 2,4-dichlorophenoxyacetic acid and arsenic alters biomarkers in rats.

2,4-dichlorophenoxyacetic acid (2,4-D) and arsenic cause severe and extensive biological toxicity in organisms. However, their interactions and toxic mechanisms in co-exposure remain to be fully elucidated. In this study, 28 four-week-old female rats were divided into four groups and exposed to 100 mg/L arsenic or/and 600 mg/L 2,4-D through drinking water for a period of 28 days. As a result, it was revealed that biochemical indicators (ALT, AST, ALP, blood urea nitrogen, and creatinine) were increased and decreased hormonal parameters (FSH, LH, PG, and E2) in arsenic and 2,4-D and arsenic combination-treated groups. Moreover, increased lipid peroxidation (malondialdehyde level) and decreased antioxidant status (superoxide dismutase and catalase activities) were found in the co-exposure groups compared with the individual-exposure groups. Meanwhile, severe DNA damage was observed in co-exposure groups. Additionally, the levels of apoptotic (Bax, Caspase-3, Caspase-8, Caspase-9, p53, and PARP) and inflammation (NFκB, Cox-2, TNF-α, and TGFßI) indexes in the co-exposure groups were markedly increased, whereas the levels of anti-apoptosis index (Bcl-2) were decreased. It was also observed that co-exposure with 2,4-D and arsenic caused more histopathological changes in tissues. Generally, these results show that co-exposure to 2,4-D and arsenic can seriously cause oxidative stress, DNA damage, apoptosis and inflammation while having toxicological risk for organisms.

Tubuloside A, a phenylethanoid glycoside, alleviates diclofenac induced hepato-nephro oxidative injury via Nrf2/HO-1.

The most prominent adverse effects of nonsteroidal anti-inflammatory drugs (NSAIDs) such as diclofenac (DF) are hepato-renal damage. Natural antioxidants can be preferred as an alternative and/or combination to improve this damage. This present study was conducted to evaluate the protective effect of Tubuloside A (TA) against diclofenac (DF)-induced hepato-renal damage. TA (1 mg/kg, ip) was administered to male Sprague-Dawley rats for 5 days, and DF (50 mg/kg, ip) was administered on Days 4 and 5. Plasma aspartate amino transferase, alanine amino transferase, alkaline phosphatase, blood urea nitrogen and creatinine were measured to evaluate liver and kidney functions. Additionally, oxidative stress parameters (malondialdehyde, glutathione, superoxide dismutase, catalase, and 8-oxo-7,8-dihydro-2'-deoxyguanosine) in blood, liver, and kidney tissues, changes in mRNA expression of genes involved in the Nrf2/HO-1 signalling pathway (Nrf2, HO-1, NQO-1, IL-6, iNOS, Cox-2, TNF-α, IL1-ß and NFκB) and apoptotic process (Bcl-2, Cas-3 and Bax) in liver and kidney tissues were determined. Additionally, tissue sections were evaluated histopathologically. Biochemical, histopathological, and molecular results demonstrated the hepato-renal toxic effects of DF, and TA treatment protected the liver and kidney from DF-induced damage. This provides an explanation for the hepato-nephro damage caused by DF and offers new ideas and drug targets together with TA for the prevention and treatment of DF injury.

Polydatin reduces aflatoxin-B1 induced oxidative stress, DNA damage, and inflammatory cytokine levels in mice.

This study showed the protective effect of polydatin (PD), which has an antioxidant activity against oxidative stress in mice caused by aflatoxin B1 (AFB1). In this study, 36 male Swiss albino mice were divided equally into 6 groups: 0.2 mL of FTS was administered to the control group, 0.2 mL of olive oil to the second group, and 0.75 mg/kg AFB1 to the third group by intragastric gavage every day for 28 days. The fourth, fifth, and sixth groups were administered 50, 100, and 200 mg/kg PD and 0.75 mg/kg AFB1 intragastrically for 28 days, respectively. AFB1 administration increased plasma aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, blood urea nitrogen, creatinine, and malondialdehyde levels in blood and tissue samples but decreased the level of glutathione and the activities of superoxide dismutase and catalase. On the other hand, it was determined that PD applications depending on the increasing doses brought these levels closer to normal. In addition, AFB1 administration increased the amount of ssDNA and liver COX-2, TNF-α, IL-6, NFκB, and Cyp3a11 mRNA expression levels; on the other hand, it decreased the IL-2 mRNA expression level. In contrast, increasing doses of PD application regulated the amount of ssDNA and these mRNA expression levels. Additionally, histopathological damage was observed in the liver and kidney tissues of the AFB1 group, while PD applications in a dose-dependent manner improved these damages. As a result, it was determined that PD reduced AFB1-induced oxidative stress, DNA damage, and inflammation and exhibited a protective effect on tissues in mice.

Boron exhibits hepatoprotective effect together with antioxidant, anti-inflammatory, and anti-apoptotic pathways in rats exposed to aflatoxin B1.

BACKGROUND: Aflatoxins are one of the important environmental factors that pose a risk to living organisms. On the other hand, it has been indicated in research that boron intake has beneficial effects on organisms. In this study, the effect of boron was disclosed in rats exposed to aflatoxin B1 (AFB1), which poses a toxicological risk. METHODS: A total of 36 male Sprague Dawley rats were separated into 6 groups and 0.125 mg/kg bw AFB1 and 5, 10, or 20 mg/kg bw doses of boron were given orally for 21 days. End of the experiment, biochemical, molecular, and histopathological analyses were performed. RESULTS: AFB1 treatment increased liver enzyme activities (AST, ALT, and ALP) and malondialdehyde level; on the other hand, it caused a decrease in glutathione level, superoxide dismutase and catalase activities. In addition, the mRNA expression levels of apoptotic (Bax, Caspase-3, Caspase-8, Caspase-9, and p53) and pro-inflammatory (TNF-α and NFκB) genes increased and the mRNA expression of the anti-apoptotic gene (Bcl-2) decreased in liver tissue. Also, AFB1 treatment increased DNA damage and caused histopathological alterations in the liver tissue. Additionally, boron applications at doses of 5, 10, and 20 mg/kg bw given with AFB1 reversed these negative changes. CONCLUSIONS: As a result, boron exhibited hepatoprotective effect together with antioxidant, anti-inflammatory, and anti-apoptotic effects against AFB1-induced liver damage.

Acetaminophen-Induced Nephrotoxicity: Suppression of Apoptosis and Endoplasmic Reticulum Stress Using Boric Acid.

Acetaminophen (APAP) is one of the popular and safe pain medications worldwide. However, due its wide availability, it is frequently implicated in intentional or unintentional overdoses where it can cause severe liver injury and even acute liver failure. Boron is a bioactive trace element, found naturally as boric acid (BA) and borate. In this study, the effects of boric acid on the acute renal toxicity induced by APAP in rats were researched in comparison with N-acetyl cysteine (NAC). In the study, 7 groups were formed and 2 g/kg dose of paracetamol per rat was prepared by suspending in 1% Carboxy Methyl Cellulose (CMC) solution of phosphate buffer saline (PBS). Boric acid dissolved in saline was administered to experimental animals by gavage at doses of 50, 100, and 200 mg/kg. In this study, ER stress and apoptosis formed by paracetamol-induced nephrotoxicity were investigated. This purpose determined iNOS, PERK, ATF6, NFkB p53, caspases 3, 12, bcl-2, and bcl-xL gene mRNA expression kidney tissue. Also, the levels of kidney injury molecule-1 (KIM-1), Cysteine (Cys), and IL-18 levels, which are mentioned today as kidney damage markers were compared with BUN and creatine levels. The effect of boron on kidney damage was determined by histopathologic. Data were statistically analyzed by using SPSS-20 ANOVA and stated as means and standard deviation. According to the data obtained in our study, we believe that boric acid has a protective effect on the negative effects of paracetamol on the kidney. We believe that our study will provide useful data to the literature on the possibility of a supplement to be used as an active compound in paracetamol for the prophylaxis of boric acid and it can also be converted into a useful product.

The effects of boron-supplemented diets on adipogenesis-related gene expressions, anti-inflammatory, and antioxidative response in high-fat fed rats.

The fatty liver syndrome caused by nutritional factors is a common cause of hepatic dysfunction globally. This research was designed to study the shielding effect of boron in rats fed a diet having high fat. Overall, 40 Wistar albino male rats were placed into one control and four treatment groups, that is, each having eight rats. Group I was provided with a standard rat diet while group II was only provided a high-fat diet for 60 days. Groups III, IV, and V were provided with 5, 10, and 20 mg/kg/day boron, respectively, by gastric gavage besides a high-fat diet for 60 days. Malondialdehyde was increased significantly in rats' blood and tissue because of high-fat diets. Glutathione was decreased significantly in blood and tissues because of a high-fat diet. Moreover, the activities of superoxide dismutase (SOD) and catalase (CAT) were decreased in the blood and tissues of the high-fat-fed rats. The genes expression for C-reactive protein, interleukin-1ß, leptin, and tumor necrosis factor-α were increased while gene expression for peroxisome proliferator-activated receptors was decreased in the liver of rats fed with a high-fat diet. Contrariwise, boron supplementation improves antioxidative response in terms of increased SOD and CAT activities, gene expression regulation, and improved anti-inflammatory activities. In a nutshell, boron has dose-dependent shielding antioxidative and tissue regenerative effects in rats.

Synergistic toxicity of ethanol and 2,4-dichlorophenoxyacetic acid enhances oxidant status, DNA damage, inflammation, and apoptosis in rats.

Clarifying the interactions between substances as a result of exposure to multiple xenobiotics and determining the impacts on health are important from the toxicological point of view. Therefore, the aim of the study was to investigate the synergistic toxic effects of ethanol and 2,4-dichlorophenoxyacetic acid (2,4-D) in male albino rats. A total number of 28 Wistar male rats were divided into 4 groups (7/each), and 2,4-D (5 mg/kg) and ethanol (3 g/kg) were administered orally to rats for 60 days, either alone or in combination. Co-administration of ethanol and 2,4-D increased liver functional enzyme levels and lipid peroxidation in blood and tissues while decreased glutathione and antioxidant enzyme activities when compared to individual applications. Furthermore, co-administration of ethanol and 2,4-D caused DNA damage as well as the increase in apoptotic and proinflammatory cytokine gene expressions. Furthermore, histopathological examination of the tissues especially liver and kidney revealed that these two substances induced more serious damage. In conclusion, co-administration of ethanol and 2,4-D resulted in strong toxic effects on tissues (especially liver) with a synergistic interaction and give rise to serious toxicological drawbacks.

Resveratrol alleviates pyraclostrobin-induced lipid peroxidation, oxidative stress, and DNA damage in rats.

Pyraclostrobin (Pyra) is a fungicide in the strobilurin class and has proven to be very toxic to organisms primarily aquatic species. Resveratrol (Res) is a phytoalexin that exhibits multiple bioactivities as anti-oxidative, anti-inflammatory, cardiovascular protective, and anti-aging and is found in plant species such as mulberry, peanut, and grape. This study aimed to determine the protective effect of Res against Pyra-induced lipid peroxidation, oxidative stress, and DNA damage in rats. For this purpose, a total of 48 male rats divided into 6 groups - 8 in each group - were exposed to 30 mg/kg Pyra by oral gavage once a day for 30 days and to three different concentrations of Res (5, 10, and 20 mg/kg) together with Pyra. Pyra administration increased liver enzyme parameters and malondialdehyde (MDA) levels whereas decreased glutathione (GSH) levels and activities of superoxide dismutase (SOD) and catalase (CAT). Also, Pyra treatment increased pro-apoptotic (Bax), apoptotic (Caspase-3, Caspase-8, and Caspase-9), pro-inflammatory (NFκB), cancer (CYP2E1), and cell regulatory (p53) gene expressions and decreased anti-apoptotic (Bcl-2) gene expression in the liver. Furthermore, DNA damage in blood and histopathological changes in the liver and kidney were observed with Pyra administration. In contrast, Res administrations in a dose-dependent manner improved Pyra-induced lipid peroxidation, oxidative and DNA damages, expression levels of these genes in the liver, and histopathological changes in the liver and kidney. Consequently, the treatment of Res, known for its anti-oxidant and protective properties, exhibited a protective effect on Pyra-induced lipid peroxidation, oxidant/anti-oxidant status, gene expressions, and DNA damage in rats.

Natural Products/Bioactive Compounds as a Source of Anticancer Drugs.

Cancer is one of the major deadly diseases globally. The alarming rise in the mortality rate due to this disease attracks attention towards discovering potent anticancer agents to overcome its mortality rate. The discovery of novel and effective anticancer agents from natural sources has been the main point of interest in pharmaceutical research because of attractive natural therapeutic agents with an immense chemical diversity in species of animals, plants, and microorganisms. More than 60% of contemporary anticancer drugs, in one form or another, have originated from natural sources. Plants and microbial species are chosen based on their composition, ecology, phytochemical, and ethnopharmacological properties. Plants and their derivatives have played a significant role in producing effective anticancer agents. Some plant derivatives include vincristine, vinblastine, irinotecan, topotecan, etoposide, podophyllotoxin, and paclitaxel. Based on their particular activity, a number of other plant-derived bioactive compounds are in the clinical development phase against cancer, such as gimatecan, elomotecan, etc. Additionally, the conjugation of natural compounds with anti-cancerous drugs, or some polymeric carriers particularly targeted to epitopes on the site of interest to tumors, can generate effective targeted treatment therapies. Cognizance from such pharmaceutical research studies would yield alternative drug development strategies through natural sources which could be economical, more reliable, and safe to use.

Potential protective effect of escin from Aesculus hippocastanum extract against cyclophosphamide-induced oxidative stress on rat tissues.

Cyclophosphamide (CP)-also known as cytophosphan-is an alkylating agent that has many side effects in humans and rats. Rats were divided into 5 different groups to evaluate the protective effect of escin (ES) obtained from the horse-chestnut plant (Aesculus hippocastanum) against acute damage induce by CP. Groups: control group, ethanol group, ES group (100 mg/kg body weight (bw) ES for 14 days by gastric gavage), ES + CP group (100 mg/kg bw ES for 14 days by gastric gavage and 75 mg/kg bw CP i.p. on 14th day), and CP group (75 mg/kg bw CP i.p. on 14th day). After the experiment was completed, blood and tissue samples (liver, kidney, heart, brain, lung, and testis) were taken from the rats under anesthesia. When the CP group was compared with the control group, an increase was observed in the level of Malondialdehyde (MDA) in blood and all tissues except the lung, but when it was given together with escin, there was a decrease except kidney and lung (P < 0.05). Glutathione (GSH) level decreased in the blood and all tissues when CP was given, whereas an increase was observed in the heart, brain, and lung when given with escin (P < 0.05). There was no statistical change in the activities of superoxide dismutase and catalase enzymes in all tissues. ES reduced CP-induced damage in all tissues except the kidney. As a result, it was determined that ES had a protective effect against CP-induced tissue damage in rats due to its antioxidant properties.

Boron, a Trace Mineral, Alleviates Gentamicin-Induced Nephrotoxicity in Rats.

The present study was considered to assess the protective effects of boron (B) on gentamicin-induced oxidative stress, proinflammatory cytokines, and histopathological changes in rat kidneys. Rats were split into eight equal groups which were as follows: control (fed with low-boron diet); gentamicin group (100 mg/kg, i.p.); B5, B10, and B20 (5, 10, and 20 mg/kg B, i.p.) groups; gentamicin (100 mg/kg, i.p.) plus B5, B10, and B20 (5, 10, and 20 mg/kg B, i.p.) groups. B was given to rats 4 days before the gentamicin treatment and B administration was completed on the 14th day. Gentamicin administration was started on the 4th day and finished on the 12th day. Gentamicin increased malondialdehyde levels, while reduced glutathione levels in the blood and kidney. Furthermore, superoxide dismutase and catalase activities of erythrocyte were decreased. Besides, serum and kidney nitric oxide and 8-dihydroxyguanidine levels were increased by gentamicin. Additionally, serum levels and kidney mRNA expressions of TNF-α, NFκB, IL-1ß, and IFN-γ were found to be the highest in the gentamicin group. Histopathologically, interstitial hemorrhage and tubular necrosis were detected in the kidneys of the gentamicin group. Nonetheless, B administration reversed gentamicin-induced lipid peroxidation, antioxidant status, and inflammation. In conclusion, B has a preventive effect against gentamicin-induced nephrotoxicity and ameliorates kidney tissues of the rat.

Protective effects of resveratrol on biomarkers of oxidative stress, biochemical and histopathological changes induced by sub-chronic oral glyphosate-based herbicide in rats.

The aim of this sub-chronic toxicity study is to determine the protective effects of Resveratrol (Res) on oxidative stress, biochemical and histopathological changes induced by glyphosate-based herbicide (GBH) in the blood, brain, heart, liver and renal tissues. A total of 28 male Wistar rats were equally divided into 4 groups so that each group included 7 rats. In the study, Group I (control group) was given normal rodent feed and tap water ad libitum. Group II (Res group) was given Res 20 mg kg-1, Group III (GBH group) was given GBH of 375 mg kg-1 to achieve 1/10 of Lethal Dose 50% (LD50), and Group IV (Res + GBH) was given Res 20 mg kg-1 and GBH 375 mg kg-1 with oral gavage once a day for 8 weeks. While GBH decreased the glutathione (GSH) levels in the blood, brain, heart, liver and renal tissues, it significantly increased malondialdehyde (MDA) levels. In contrast, the aforementioned parameters were seen to recover in the group to which Res was administered. Moreover, it was observed that Res improved the histopathological changes induced by GBH in rat tissues. In conclusion, Res prevents oxidative stress caused by GBH by preventing lipid peroxidation (LPO) and boosting the antioxidant defense system and decreases the damage in the brain, heart, liver and renal tissues of Wistar rats.

Bisphenol-A induced oxidative stress, inflammatory gene expression, and metabolic and histopathological changes in male Wistar albino rats: protective role of boron.

Bisphenol A (BPA) is one of the most produced chemicals in the world and has been widely employed in the food industry. Continuous and widespread exposure to BPA through drinking water and food leads to health concerns for humans. This study evaluated the effects of boron (B) on BPA-mediated oxidative stress in male Wistar albino rats. Rats were equally divided into 5 groups; corn oil was given orally to the control group; 25 mg kg-1 of BPA dissolved in corn oil was given orally to the second group. All other groups received the same dose of BPA and different doses of B (5, 10, and 20 mg kg-1 per day, respectively) orally for 30 days. The administration of BPA significantly decreased glutathione levels and increased malondialdehyde levels in rat tissues. Furthermore, BPA treatment reduced the catalase and superoxide dismutase activities in tissues and erythrocytes. Also, mRNA expression levels of TNF-α, IL-1ß, and IL-6 in the brain, liver, and testes of rats were augmented, whereas IL-10 was decreased with BPA treatment. Besides, BPA treatment adversely altered biochemical parameters and caused damage to the cell integrity of rat tissues. However, B administration reversed BPA-induced alterations in rat tissues in a dose-dependent manner. Furthermore, B exhibited antioxidant and anti-inflammatory effects and regulated metabolic and histopathological alterations in male Wistar albino rats exposed to BPA.

Antioxidant and cytoprotective effects of N-acetylcysteine against subchronic oral glyphosate-based herbicide-induced oxidative stress in rats.

It is claimed that oxidative stress has a prominent role in the mechanism of toxic effects formed by glyphosate-based herbicide (GBH) in living systems. A strong thiol compound, N-acetylcysteine (NAC), has antioxidative and cytoprotective properties. The objective in this subchronic toxicity study was to identify the prophylactic effect of NAC over histopathological changes and oxidative stress induced by GBH in blood, renal, liver, cardiac, and brain tissues. A sum of 28 male Wistar rats were divided into four equal groups, each containing 7 rats. During the study, group I (control group) was supplied with normal rodent bait and tap water ad libitum. The applied agents were 160 mg/kg NAC to group II, 375 mg/kg as equivalent to 1/10 of lethal dose 50% (LD50) of GBH to group III, and 160 mg/kg of NAC and 375 mg/kg of GBH together once per day as oral gavage to group IV for 8 weeks. While GBH decreased the levels of GSH in blood, liver, kidney, and brain tissues, it considerably increased malondialdehyde levels. On the contrary, these parameters happened to improve in the group supplied with NAC. Besides, it was seen that NAC was observed to improve the histopathologic changes in rat tissues induced by GBH. It was concluded that NAC protects oxidative stress and tissue damage induced by GBH in blood and tissue and this prophylactic effect could be attributed to its antioxidant and free radical sweeper character.

Boron ameliorates arsenic-induced DNA damage, proinflammatory cytokine gene expressions, oxidant/antioxidant status, and biochemical parameters in rats.

Arsenic, an element found in nature, causes hazardous effects on living organisms. Meanwhile, natural compounds exhibit protective effects against hazardous substances. This study evaluated the effects of boron against arsenic-induced genotoxicity and altered biochemical parameters in rats. Thirty-five male Wistar albino rats were equally divided into five groups, and the experimental period lasted 30 days. One group was used as the control, and another group was treated with 100 mg/L arsenic in drinking water. The other groups were orally treated with 5, 10, and 20 mg/kg boron plus arsenic (100 mg/L via drinking water). Arsenic caused changes in biochemical parameters, total oxidant/antioxidant status, and DNA damage in mononuclear leukocytes. Moreover, it increased IFN-γ, IL-1ß, TNF-α, and NFκB mRNA expression levels in rat tissue. However, boron treatment improved arsenic-induced alterations in biochemical parameters and increases in DNA damage and proinflammatory cytokine gene expressions.

Boron enhances early embryonic gene expressions and improves fetal development of rats.

Boron is present as several different components in nature. Besides its industrial use, it is an essential element and is playing a very important role in the metabolism. In this study, it was aimed to determine the in vivo effects of boron on mRNA expression of HEX, NANOG, and OCT-3/4 genes in embryo and histological changes during fetal development. Therefore, totally 60 female rats were allocated into 5 equal groups. Experimental groups are as the followings; positive control (fed with standart rat diet), negative control (fed with boron free diet), low boron group (fed with boron free diet and given 0.04 µg boron/ml via gastric gavage), marginal boron group (fed with boron free diet and given 0.3 µg boron/ml via gastric gavage) and normal boron group (fed with boron free diet and given 2 µg boron/ml via gastric gavage). Experimental period was performed for 14 days. Embryos were collected after 4 days of mating and the expression and protein levels of early embryonic genes namely HEX, NANOG, and OCT-3/4 were determined by using Real-Time PCR. Also, 10-20 day embryo and fetus development were histologically determined. According to the results, mRNA expression and protein levels of early embryonic genes were increased in boron groups while decreased in boron deficient group. Histopathologically, tissue and organ developments were definitely observed in the boron groups. In conclusion, mRNA expression levels of early embryonic genes decreased in boron deficient group and boron has an important role for fetal development.

The subchronic exposure to malathion, an organophosphate pesticide, causes lipid peroxidation, oxidative stress, and tissue damage in rats: the protective role of resveratrol.

The present study was planned to evaluate the protective role of resveratrol (Res) against subchronic malathion exposure in rats over four weeks. In total, 48 Wistar rats were used and divided equally into six groups. The groups were designed as the control group (received only a rodent diet and tap water), the corn oil group (0.5 ml corn oil by the oral route), and the malathion group (100 mg kg-1 day-1 by the oral route). Other three groups received malathion (100 mg kg-1 day-1) plus Res (5, 10, and 20 mg kg-1 day-1, respectively) by the oral route. Malathion increased malondialdehyde and 8-OHdG levels, whereas it decreased glutathione levels. Also, acetylcholinesterase, superoxide dismutase, and catalase activities were found to be low in the blood, liver, kidney, heart, and brain tissues. Biochemical parameters were not notably changed in all groups. In contrast, Res treatment inverted malathion-induced oxidative stress, lipid peroxidation, and activity of enzymes. Additionally, malathion-induced histopathological changes in the liver, kidney, heart, and brain were ameliorated by Res treatment. These results demonstrate that malathion increases oxidative stress and decreases the antioxidant status while Res has a protective function against malathion toxicity in rats.

The ameliorative effects of boron against acrylamide-induced oxidative stress, inflammatory response, and metabolic changes in rats.

Acrylamide (ACR) is a hazardous substance associated with the accumulation of excessive reactive oxygen species and causes oxidative stress. Presence of ACR in foods leads to public health concerns due to its known neurotoxic, genotoxic, and carcinogenic effects. The present study investigated the ameliorative effects of boron (B) against ACR exposed rats. Forty Wistar albino male rats, fed with low-boron diet, were randomly and equally allocated into 5 groups. The control group was orally treated with physiological saline as placebo, the second group was orally given 15 mg/kg ACR. The other groups were orally treated with 15 mg/kg ACR and B at the levels of 5, 10, and 20 mg/kg/day for 60 days, respectively. ACR-treatment significantly increased malondialdehyde levels whereas decreased glutathione levels in rat tissues. Also, ACR-treatment increased the activities of superoxide dismutase and catalase in erythrocytes and tissues. Meanwhile, mRNA expression levels of NFĸB, IFN-γ, IL-1ß, and TNF-α in liver and brain of rats were increased under ACR treatment. Additionally, ACR caused a significant decrease in the level of high-density lipoprotein, with increase in the levels of low-density lipoprotein, triglyceride, cholesterol, glucose, urea nitrogen, and creatinine. Lastly, B alleviated histopathological alterations induced by ACR in rat tissues.