Furan induced ovarian damage in non-diabetic and diabetic rats and cellular protective role of lycopene.

PURPOSE: In our work, furan, lycopene, and furan + lycopene treatments were applied to non-diabetic and diabetic female rats via gavage. METHODS: Ovarian tissue alterations with histopathology, immunohistochemistry, malondialdehyde levels, oxidative stress parameters such as superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase and harmful effect on ovarian tissue DNA were evaluated in all groups for 28 days. RESULTS: Furan caused the changes histological, ovarian cell's DNA structure, malondialdehyde levels, antioxidant enzymes activities as in a statistically significant manner in each group. Useful effect of lycopene was determined both in non-diabetic and diabetic treatment groups against furan according to the used experimental parameters. Although some histopathological alterations were seen in diabetic and non-diabetic/diabetic plus furan-treated group's ovarians, lycopene restored these variations near to normal levels in furan + lycopene treated groups for in 28 days. Additionally, the results of our immunohistochemical analysis and alterations of the oxidative stress parameters results also supported these findings. CONCLUSIONS: Our result confirms that lycopene has protective effect and significantly altered diabetes and furan-induced toxicity in the rat ovarian tissue.

Protective Effects of Lycopene on Furan-treated Diabetic and Non-diabetic Rat Lung.

We assessed the effects of furan and lycopene on the histopathological and biochemical changes on lungs, body and lung weights, and food consumption of rats. Furan and diabetes caused histopathological changes, increment in malondialdehyde levels, and decrease in antioxidant enzyme activities. Lycopene showed a protective effect against these damages, except for glutathione-S-transferase and glutathione peroxidase activities. Consequently, furan and diabetes resulted in lung toxicity. Our findings demonstrate that furan treatment resulted in more alterations in histology and biochemical parameters in diabetic rats and lycopene showed protective effects against these alterations.

Protective role of catechin and quercetin in sodium benzoate-induced lipid peroxidation and the antioxidant system in human erythrocytes in vitro.

The aim of this study was to evaluate the protective effect of catechin and quercetin in sodium benzoate- (SB-) induced oxidative stress in human erythrocytes in vitro. For this, the effects of SB (6.25, 12.5, 25, 50, and 100 µg/mL), catechin (10 µM), and quercetin (10 µM) on lipid peroxidation (LPO) and the activities of SOD, CAT, GPx, and GST were studied. Significantly higher LPO and lower activities of antioxidant enzymes were observed with the increasing concentrations of SB. Catechin or quercetin protected the erythrocytes against SB-induced toxicity only at low concentrations of SB. The presence of catechin or quercetin at 10 µM have no effect on SB-induced toxicity at high concentrations of SB (50 and 100 µg/mL). In conclusion, SB may cause oxidative stress as food additive in human erythrocytes in vitro. So, it appears that our findings provide evidence for the protection of erythrocytes from SB that could be considered for further studies.

In vitro effects of quercetin on oxidative stress mediated in human erythrocytes by benzoic acid and citric acid.

Benzoic acid (BA) and citric acid (CA) are food additives commonly used in many food products. Food additives play an important role in food supply but they can cause various harmful effects. The in vitro adverse effects of BA and CA and the protective effect of quercetin on human erythrocytes were investigated by measuring malondialdehyde (MDA) levels and superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) activities. Erythrocytes were incubated with BA and CA, at three doses of 50, 100 and 200 microg/ml, and quercetin, at a concentration of 10 microM. After BA and CA application, a dose-dependent increase in MDA level and decreases in SOD, CAT, GST and GPx activities were found in erythrocytes. Among the two food additives, BA exerted a more harmful influence on human erythrocytes than CA. The protective effects of quercetin against oxidative stress--induction in the human erythrocytes by CA and BA, were found when these two food additives were applied at each of three doses of 50, 100 and 200 microg/ml. However, complete protection of quercetin against CA toxicity was only observed when this agent was applied at a lower dose of 50 microg/ml. Quercetin did not completely protect erythrocytes even at the lowest concentration of BA.

Protective role of vitamins C and E in dichlorvos-induced oxidative stress in human erythrocytes in vitro.

Organophosphate (OP) pesticides such as dichlorvos (DDVP) intoxication has been shown to produce oxidative stress due to the generation of free radicals, which alter the antioxidant defense system in erythrocytes. In this study, the effects of DDVP (1, 10, 100 µM) or DDVP + vitamin C (VC; 10 µM) or vitamin E (VE; 30 µM), on the levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities in human erythrocytes were examined in vitro. There were no statistical differences between all groups for 1 µM concentration of DDVP. Treatment with DDVP alone produced an increase in the level of MDA and decreased activities of antioxidant enzymes (P < 0.05). Groups treated with vitamins and DDVP showed protective effects of vitamins against DDVP-induced changes in antioxidant enzyme activity and lipid peroxidation (LPO) (10 µM). At 100 µM concentration of DDVP vitamins had no effect on DDVP-induced toxicity. The results show that administration of DDVP resulted in the induction of erythrocyte LPO and alterations in antioxidant enzyme activities, suggesting that reactive oxygen species (ROS) may be involved in the toxic effects of DDVP. Also the data show that the plasma level of VC and VE may ameliorate OP-induced oxidative stress by decreasing LPO in erythrocytes at certain doses of OP pesicides.

Investigation of protective effects of apilarnil against lipopolysaccharide induced liver injury in rats via TLR 4/ HMGB-1/ NF-κB pathway.

Sepsis caused by infection is one of the most important problems of clinical medicine. This study aimed to determine the effect of Apilarnil (API), a bee product, on lipopolysaccharide (LPS) induced liver injury. In the study, 64 adult Sprague-Dawley rats were divided into eight groups; control, 0.2, 0.4 and 0.8 g / kg apilarnil (API) treated groups, LPS (30 mg / kg) group, LPS + 0.2, LPS + 0.4 and LPS + 0.8 g / kg API. At tissues obtained from rats, histopathological evaluation, biochemical analysis by ELISA (Catalase-CAT, malondialdehyde-MDA, superoxide dismutase-SOD, xanthine oxidase-XOD, and testican 1-TCN-1), immunohistochemical evaluation (Toll-like receptor 4 (TLR4), High Mobility Group Box Protein 1 (HMGB-1), nuclear factor kappa B (NF-κB), Tumor necrosis factor-alpha (TNF-α), Interleukin 1 beta (IL-1ß), Interleukin 6 (IL-6) and Inducible nitric oxide (iNOS)), TUNEL analysis to determine the number of apoptotic cells and Comet test as an indicator of DNA damage were performed. Histopathological examination revealed dilated blood vessels, inflammatory cell infiltration, and pyknotic nuclei damaged hepatocytes in the liver tissues of the LPS group. It was found that tissue damage was decreased significantly in LPS + API treatment groups compared to the LPS group. The number of TUNEL positive cells observed in the LPS group in liver samples increased compared to control and API-treated groups only (p < 0.05). The number of TUNEL positive cells showed a statistically significant decrease compared to the LPS group in the groups treated with LPS + API. LPS treatment increased MDA, XOD, and TCN 1 levels and decreased SOD and CAT levels; this effect was reversed in the groups treated with LPS + API. In the LPS group, DNA damage was significantly increased when compared with the LPS + API. LPS treatment increased expression of TLR4, HMGB-1, NF-κB, iNOS, TNF-α, IL-1ß, IL-6; in the groups treated with LPS + API reduced this increase. In conclusion, apilarnil administered in rats may be thought to prevent LPS-induced liver damage by inhibiting the TLR4 / HMGB-1 / NF-κB signaling pathway.

Furan-induced cardiotoxicity in diabetic rats and protective role of lycopene.

The objective of this current study is to search the impacts of furan and lycopene on a diabetic rat's heart. Diabetes increases prevalence with a sedentary lifestyle and obesity. Furan, a carcinogen, was detected in foods that had undergone thermal treatment. Two groups were formed, such as: the control and diabetic groups. Diabetic groups fall into four allocated groups: control, lycopene, furan, and furan + lycopene. The changes in malondialdehide levels, antioxidant enzymes' activities, and histopathology of the heart were pointed out. We observed that the changes in both the MDA level and the antioxidant enzymes' activities were due to diabetes. Furan-induced increment in MDA levels, but GST, CAT, SOD, and GPx activities showed a decrease. Lycopene influenced these changes positively. In terms of the pathological studies, changes were also observed in diabetic rats. The histological damage in the diabetic furan groups was found to be very serious. Lycopene was protective against furan that caused histopathological changes. Diabetes and furan resulted into heart damages in rats and lycopene showed preventive effects. But this was not a complete protection. PRACTICAL APPLICATIONS: Furan by product of chlorinated chemical compounds production and chemical processes including combustion, are virtually ubiquitous in the environment. Because of this, furan occur potential risk for human health. Furan is known to exist at higher levels in fatty foods, such as full-fat milk and dairy products, meat and eggs. They can accumulate in the fatty tissues of animals and humans. Diabetes increase in the prevalence of a sedentary lifestyle and obesity. Diabetes with furan-induced cardiotoxicity. Foods should not be heated over and over again, especially diabetic heart patients should stay away from this situation.

Acute toxic effect of lipopolysaccharides to blood tissue in rats and responses to vitamin E and sodium selenite.

This work has been prepared to find out changes in the biochemicals with DNA damage, micronucleus, and apoptosis to lipopolysaccharides (LPS) alone or vitamin E (VE) and sodium selenite (SS) in rats' blood tissue. Rats were divided into eight groups according to the treatment into control vitamin E (VE) treatment group (200 mg/kg bw), sodium selenite (SS) treatment (0.35 mg/kg bw) group, VE + SS treatment group (200 + 0.35 mg/kg bw), LPS treatment group (10 mg/kg bw), LPS + VE (10 + 200 mg/kg bw), LPS + SS treatment (10 + 0.35 mg/kg bw), and LPS + SS+VE treatment (10 + 0.35 + 200 mg/kg bw) group for 6 hr. LPS increased malondialdehyde (MDA) level and decreased antioxidant enzymes' activities in rat erythrocytes and leukocytes. DNA damage of leukocytes with comet assay and RAPD-PCR was detected in LPS treatment group. The levels of micronucleus and apoptosis percentage were increased significantly at the end of 6 hr. VE and/or SS protected the LPS-induced erythrocytes and leukocytes against damage as they have caused amelioration of rats by altering the results. As a result, the co-administration of VE and/or SS against LPS-induced damage provides protection. VE and/or SS in patients and animal models with sepsis must be taken in the diet because they are protective against the cellular degradation caused by oxidative damage. PRACTICAL APPLICATIONS: LPS obtained from E. coli is used more frequently in experimental sepsis studies. When LPS is administered to experimental animals, interstitial pneumonia, adult respiratory fatal syndrome, acute tubular necrosis, and fatal effects such as coagulopathy and hypoglycemia may be seen in these animals. The co-treatment of VE and SS may be more effective than using them alone against LPS.

All aspect of toxic effect of brilliant blue and sunset yellow in Allium cepa roots.

Substances added to food are considerable for survival and are the oldest technologies used in preservation, sweetening and coloring. This work was conducted to evaluate the toxicity of the food additives sunset yellow (SY) and brilliant blue (BB) on Allium cepa root meristematic cells. Control and treatment groups were created from germinated roots. Group 1 (control group) did not receive chemicals. Group 2 (SY or BB-treatment group), received increasing doses of SY (25, 50, 100 and 500 ppm) and BB (100, 200, 400 and 500 ppm) with time periods of 24, 48 and 72 h. After different treatment periods, the roots were obtained from all groups and EC50 concentrations, cell death, chromosome aberrations, mitotic index were observed by a light microscopy. Changing antioxidant capacity of roots was determined by FRAP and TEAC assay. Also, DNA damage was measured by comet assay and RAPD-PCR technique. Approximately 50 and 200 ppm were accepted as EC50 value for SY and BB, respectively. Chromosome aberration values were obtained with increasing concentrations and longer treatment times such as chromosome bridge, C-mitosis, micronucleus, chromosome mis-segregation in both groups. Increasing exposure doses of SY and BB caused decreasing mitotic index values at 72 h. FRAP and TEAC assay showed that antioxidant capacity of roots was decreased by increasing concentrations of SY and BB. The tail DNA% and tail length significantly increased for all exposure times when compared to the control group. 50 and 200 ppm of SY and BB caused a genotoxic effect on genetic material at 72 h according to RAPD-PCR. Increasing the doses of SY and BB resulted in increased toxicity to all studied parameters of A. cepa. In conclusion, the SY and BB tested in this study have cytotoxic and mutagenic potential. Furthermore, SY is more harmful than BB for use in the A. cepa root meristematic cells.

Assessment of anticytotoxic effect of lichen Cladonia foliacae extract on Allium cepa root tips.

The aim of this study is to investigate the protective effect of lichen Cladonia foliacae (Huds.) (CF) on hydrogen peroxide (H2O2)-induced toxicity through cell death, chromosome aberrations, mitotic index, oxidative stress parameters, and DNA damage in a Allium cepa root meristematic cells. Any chemical was not given for control group. Two doses of H2O2 (3 and 7%) were given to the roots for 1 h and the root tips were treated with CF water extract (50 and 100 µL) with increasing times for treatment groups. The roots were taken from control and treatment groups, and mitotic index, cell death, and chromosome aberrations were performed by light microscope. Changing antioxidant capacity of roots was revealed by FRAP and TEAC assay. Also, DNA damage was measured by comet assay and RAPD-PCR technique. Chromosome aberration values were obtained with increasing concentrations with longer treatment times, such as chromosome bridge, vagrant, and polyploidy in both groups. Increasing exposure doses of H2O2 caused decreasing mitotic index values at 72 h. TEAC and FRAP assay demonstrated that roots' capacity of antioxidant was altered by increasing concentrations of H2O2. The tail DNA% and tail length significantly increased in all exposure times when compared to control group. Three and seven percent of H2O2 caused the genotoxic effect on genetic material at 72 h according to RAPD-PCR technique. Increasing the doses of H2O2 resulted in increased toxicity to all studied parameters of A. cepa, but CF extract altered all changing parameters of A. cepa root cell. The H2O2 tested in this study have cytotoxic and mutagenic potential, but extract of CF was protective against H2O2 caused toxicological changes. But, it did not protect completely in the A. cepa root meristematic cells.

Hepatoprotective effects of capping protein gelsolin against hyperoxia-induced hepatotoxicity, oxidative stress and DNA damage in neonatal rats.

Tissues and organs get exposed to high oxygen (O2) supply in hyperoxia conditions. The goal of this research was to investigate the protective effect of actin binding protein gelsolin on hyperoxia-induced hepatotoxicity through histopathology and measurement of oxidative stress parameters and DNA damage in a neonatal Wistar albino rats. The pups were randomly separated to four equal groups such as: normoxia control group (NC), normoxia plus gelsolin group (NG, 10 ng/kg bw/day gelsolin), hyperoxia (≥85% O2) group (HC), hyperoxia plus gelsolin group (HG, ≥85% O2; 10 ng/kg bw/day gelsolin). Histopathological changes of pups in hyperoxia condition were revealed in the form of severe leukocyte infiltration, vascular congestion, necrosis, vacuolar degeneration, binucleated hepatocytes and hemorrhage in the liver tissue. SOD, CAT, GPx and GST activities decreased and MDA level increased in the hyperoxia-induced group in liver tissue (P < 0.05). Tail DNA%, tail length and moment indicating DNA damage statistically increased in hyperoxia treatment groups when compared to controls. Treatment of rats with hyperoxia plus gelsolin prevented hyperoxia-induced changes in tissue structure, antioxidant enzyme activities and MDA level, mean tail DNA% and length. Based on these findings, gelsolin restored these changing to near normal levels but it does not protect completely in the hyperoxia conditions.

DNA damage in human germ cell exposed to the some food additives in vitro.

The use of food additives has increased enormously in modern food technology but they have adverse effects in human healthy. The aim of this study was to investigate the DNA damage of some food additives such as citric acid (CA), benzoic acid (BA), brilliant blue (BB) and sunset yellow (SY) which were investigated in human male germ cells using comet assay. The sperm cells were incubated with different concentrations of these food additives (50, 100, 200 and 500 µg/mL) for 1 h at 32 °C. The results showed for CA, BA, BB and SY a dose dependent increase in tail DNA%, tail length and tail moment in human sperm when compared to control group. When control values were compared in the studied parameters in the treatment concentrations, SY was found to exhibit the highest level of DNA damage followed by BB > BA > CA. However, none of the food additives affected the tail DNA%, tail length and tail moment at 50 and 100 µg/mL. At 200 µg/mL of SY, the tail DNA% and tail length of sperm were 95.80 ± 0.28 and 42.56 ± 4.66, for BB the values were 95.06 ± 2.30 and 39.56 ± 3.78, whereas for BA the values were 89.05 ± 2.78 and 31.50 ± 0.71, for CA the values were 88.59 ± 6.45 and 13.59 ± 2.74, respectively. However, only the highest concentration of the used food additives significantly affected the studied parameters of sperm DNA. The present results indicate that SY and BB are more harmful than BA and CA to human sperm in vitro.

Furan-induced hepatotoxic and hematologic changes in diabetic rats: the protective role of lycopene.

Furan forms as a result of thermal treatment of food and induces harmful effects on organisms. In our work, lycopene, furan, and a combination of the two were given to diabetic male rats for 28 days. Hematological changes, total protein and cholesterol, triglyceride, and albumin levels, alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, and alkaline phosphatase activities of the serum, malondialdehyde levels, glutathione peroxidase, catalase, glutathione-S-transferase, superoxide dismutase activities, DNA damage in liver tissues and hepatic histopathological alterations were compared to a control group. There were significant changes in the liver function tests, DNA damage, activities of antioxidant enzymes, and malondialdehyde levels between diabetic control and non-diabetic control groups, between diabetic control and diabetic lycopene groups, and also between diabetic furan and diabetic control groups. In diabetic lycopene and diabetic furan + lycopene treated groups we designated the preventive effects of lycopene against diabetes and furan, however, on the analysed parameters only. In spite of some pathological alterations designated in diabetic furan treated group's liver, fewer pathological alterations were observed in furan+lycopene treated groups at the end of week 4. Consequently, lycopene significantly reduced furan- and diabetes-induced toxicity in rat liver.

Furan toxicity on testes and protective role of lycopene in diabetic rats.

OBJECTIVE: Furan (C4H4O) is a heat-induced food contaminant that is utilized as an industrial chemical agent. Lycopene is a natural substance that is produced by plants and tomatoes. We aimed to evaluate the toxicity of furan on testes and the protective effect of lycopene in diabetic rats. MATERIAL AND METHODS: Male Wistar albino rats were divided into five groups: Group 1 (control group) received 1 mL/kg corn oil. Group 2 (diabetic control group) received 55 mg/kg STZ and 1 mL/kg corn oil. Group 3 (diabetic lycopene group) received 55 mg/kg STZ and 4 mg/kg lycopene. Group 4 (diabetic furan group) received 55 mg/kg STZ and 40 mg/kg furan. Group 5 (diabetic furan + lycopene group) received 55 mg/kg STZ, 40 mg/kg furan, and 4 mg/kg lycopene. After 28 days, the testes were extirpated in all groups. In the testicular tissue samples, the level of malondialdehyde (MDA) and the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and reducted glutathione (GST) were studied. Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), and testosterone levels were measured. Histopathologic examination was performed by light microscope. RESULTS: The MDA level and the activities of CAT, GPx, SOD, and GST were found to be higher in the furan group than in the control and diabetic control groups (p<0.05). The MDA level and the activities of CAT, GPx, SOD, and GST were significantly lower in the furan + lycopene group than in the furan group (p<0.05). CONCLUSION: The low blood testosterone level in the rats who received furan suggested the presence of endocrinological defects and cellular degenerative changes. Lycopene may be effective to reverse furan toxicity in diabetic rat testes.

Protective effect of (-)-epigallocatechin-3-gallate on capsaicin-induced DNA damage and oxidative stress in human erythrocyes and leucocytes in vitro.

The aim of this study is to show that protective effects of the main catechin (-)-epigallocatechin-3-gallate (EGCG) against capsaicin (CAP) induced oxidative stress and DNA damage in human blood in vitro. Superoxide dismutase, catalase, glutathione peroxidase and malondialdehyde (MDA) level were studied in erythrocytes and leucocytes with increased concentrations of CAP. DNA damage in leucocytes was measured by the comet assay. Human blood cells have been administered with doses between 0 and 200 µM of CAP and/or EGCG (20 µM) for an hour at 37 °C. Treatment with CAP alone has increased the levels of MDA and decreased antioxidant enzymes in human blood cells. A significant increase in tail DNA%, mean tail length and tail moment indicating DNA damage has been observed at the highest dose of CAP treatment when compared to controls. Treatment of cells with CAP plus EGCG prevented CAP-induced changes in antioxidant enzyme activities and MDA level and mean tail lenght indicating DNA damage. A significant increase in mean tail lenght was observed at high doses of CAP. These data suggest that EGCG can prevent toxicity to human erythrocytes and leucocytes caused by CAP, only at low doses.

Effects of lead nitrate and sodium selenite on DNA damage and oxidative stress in diabetic and non-diabetic rat erythrocytes and leucocytes.

The adverse effects of lead nitrate (LN) and the preventive role of sodium selenite were investigated in diabetic and non-diabetic rat blood by measuring trolox equivalent antioxidant capacity (TEAC), ferric reducing antioxidant power (FRAP), malondialdehyde (MDA) levels and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) also by evaluating DNA damage with comet assay. LN increased the levels of MDA, tail DNA%, mean tail length and tail moment, decreased the enzymes activities, FRAP and TEAC values. In sodium selenite+LN group, we observed the protective effect of sodium selenite on examining parameters. Diabetes caused alterations on these parameters, too. We found that sodium selenite did not protect against diabetes caused damages. As a result, LN caused toxic effects on blood cells and sodium selenite alleviated this toxicity but it did not show preventive effect against diabetes. Also, LN caused more harmfull effects in diabetic groups than non-diabetic groups.

Protective effect of bilberry (Vaccinium myrtillus L.) on cisplatin induced ovarian damage in rat.

Cisplatin is one of the most effective chemotherapeutic agents but injury may occur at higher doses. The aim of this study was to investigate the effect of bilberry on cisplatin induced toxic effects in rat ovary. Twenty-one female Wistar-Albino rats were utilized to form three groups: In group 1 (control group), each rat received intraperitoneal injection of 1 mL of 0.9 % NaCl saline solution during 10-days. In group 2 (cisplatin group), a single dose of 7.5 mg/kg b.w. cisplatin was given. In group 3 (cisplatin + bilberry group), a single dose of 7.5 mg/kg cisplatin and bilberry at 200 mg/kg b.w. were given for 10 days. Ovaries were surgically removed in all groups and prepared for biochemical and light microscopic investigations at the examination times. Malondialdehyde (MDA) levels and activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) of tissue samples were measured. Histopathological damages in cisplatin administrated rats were seen such as severe edema, vascular congestion, hemorrhage and follicular degeneration in the ovary tissue. Moderate pathological alterations were observed in rats treated with bilberry plus cisplatin. Cisplatin administration significantly increased MDA production and decreased SOD, CAT, GPx and GST activities in the ovarian tissue when compared to the control group (p < 0.05). Cisplatin + bilberry administration increased antioxidant enzymes activities and reduced MDA levels. Bilberry administration seems to reduce the cisplatin induced ovarian toxicity thus it alleviates free radical damage. But it dose not protect completely rat ovary tissues.

Assesment of the Genotoxic Effect of the Diazinon on Root Cells of Allium cepa (L.)

ABSTRACT Organophosphorous pesticides (OPs) posses a great potential of acute toxicity for exposed animals and men. To evaluate the toxic potential of the organophosphate diazinon on root meristematic cells of Allium cepa L., was created two groups: In group 1 (control group), was not given any chemical. In group 2 (diazinon-treatment group), different doses (10, 40, 80 and 160 ppm) and times periods (24, 48 and 72 h) were administered. After exposure, cell death, effective concentration (EC50), mitotic index, cellular /chromosome aberrations, DNA damage by comet assay and RAPD-PCR were assessed at exposure times. EC50 value of diazinon was detected approximately 80 ppm. Hyperchromasia, later segragation, micronucleus, pulverised nucleus, nuclear cytoplasmic shrinkage and cell death, cytoplasmic vacuolation were detected in meristem cells as chromosome/celular aberrations for 72 h at 80 ppm. DNA damage was identified using tail DNA%, tail lengths and tail moment from these cells. Increasing exposure doses of diazinon caused increasing tail DNA% and tail lengths at 72 h. DNA bands of increasing concentrations treated groups were more distant to compare with the control group according to RAPD-PCR method. Diazinon cause cytotoxic and genotoxic on A. cepa root and could be considered for further toxicological evaluations.

Lycopene Protects the Diabetic Rat Kidney Against Oxidative Stress-mediated Oxidative Damage Induced by Furan

Furan is a food and environmental contaminant and a potent carcinogen in animals. Lycopene is one dietary carotenoid found in fruits such as tomato, watermelon and grapefruit. The present study was designed to explore the protective effect of lycopene against furan-induced oxidative damage in streptozotocin (STZ)-induced diabetic rat kidney. At the end of the experimental period (28 days), we found that lycopene markedly decreased the malondialdehide (MDA) levels in the kidney, urea, uric acid and creatinine levels in the serum of furan-treated rats. The increase of histopathology in the kidney of furan-treated rats were effectively suppressed by lycopene. Furthermore, lycopene markedly restored superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) activities in the kidney of furan-treated rats. In conclusion, these results suggested that lycopene could protect the rat kidney against furan-induced injury by improving renal function, attenuating histopathologic changes, reducing MDA production and renewing the activities of antioxidant enzymes.

Assessment of the DNA Damage in Human Sperm and Lymphocytes Exposed to the Carcinogen Food Contaminant Furan with Comet Assay

ABSTRACTThe aim of this work was to assess the damage of DNA in human blood cell and spermin vitro under the influence of furan. These cells were administered 0-600 μM of furan at 37 and 32oC for 30 and 60 min, respectively. A significant increase in tail DNA%, tail length and moment indicating DNA damage was observed at increasing doses when compared to the controls. The treatment with 300 and 600 μM of furan showed a maximum increase of 86.74 ± 2.43 and 93.29 ± 8.68 compared to the control tail DNA% in lymphocytes. However, only 600 μM of furan showed a maximum increase of 94.71 ± 6.24 compared to the control tail DNA% in sperm. The results suggested that furan caused DNA damage in lymphocytes at increasing doses, but appeared to have not the same effect on human sperm at the low doses. Genotoxic activity had an impact on the risk assessment of furan formed on the food for human cells. Therefore, it would be important to further investigate these properties of furan as the food mutagen.