Nurhayat Barlas

Influence of vitamin C on bisphenol A, nonylphenol and octylphenol induced oxidative damages in liver of male rats.

The purpose of this study was to investigate whether bisphenol A (BPA), nonylphenol (NP) and octylphenol (OP) induce oxidative stress in the liver of male rats and co-administration of vitamin C can prevent any possible oxidative stress. Wistar male rats were divided into seven groups (vehicle, BPA, NP, OP, BPA+C, NP+C, OP+C). BPA, OP and NP groups (25 mg kg(-1)day(-1)) were administered orally to rats three times a week for 50 days. In BPA+C, NP+C, OP+C groups, vitamin C (60 mg kg(-1)day(-1)) was administered along with BPA, OP and NP (25 mg kg(-1)day(-1)) treatments. Aspartate transaminase (AST), alanine transaminase (ALT), lactate dehydrogenase (LDH), thiobarbituric acid-reactive substances (TBARS) were increased, glutathione (GSH) levels were decreased in treatment groups. AST, ALT, LDH and TBARS levels were increased whereas GSH levels were decreased in BPA+C, NP+C and OP+C groups compared to BPA, NP, and OP groups, respectively. Hepatic necrosis and congestion were observed in livers of rats treated. In conclusion, the present results demonstrate that BPA, NP, and OP cause oxidative damage by disturbing the balance between ROS and antioxidant defenses system in liver of male rats. Vitamin C co-administration along with BPA, NP, OP aggravates the damage in liver of male rats.

The effect of vitamin C on bisphenol A, nonylphenol and octylphenol induced brain damages of male rats.

Bisphenol A (BPA), nonylphenol (NP) and octylphenol (OP) are endocrine-disrupting chemicals that has been shown to exert both toxic and estrogenic effects on mammalian cells. The aim of this study was to investigate if BPA, NP and OP induce oxidative stress on the brain tissue of male rats and if co-administration of vitamin C, an antioxidant, can prevent any possible oxidative stress. The male rats were divided into seven groups as control (vehicle), BPA, NP, OP, BPA+C, NP+C, OP+C. BPA, OP and NP (25 mg/(kg day)) were administrated orally to male Wistar rats for 45 days. In vitamin C co-administration groups (BPA+C, NP+C, OP+C), vitamin C (60 mg/(kg day)) were administrated orally along with BPA, OP and NP (25 mg/(kg day)) treatments. The rats in the control group received olive oil orally. The final body and absolute organ weights of treated rats did not show any significant difference when compared with the control group. Also, there were no significant difference in relative organ weights of BPA, NP, OP, BPA+C and NP+C groups when compared with control group. Only, relative organ weights were increased significantly in OP+C group compared with control group. Decreased levels of reduced glutathione (GSH) were found in the brains of BPA, NP, OP treated rats. The end product of lipid peroxidation, malondialdehyde (MDA), appeared at significantly higher concentrations in the BPA, NP, and OP treated groups when compared to the control group. On the other hand, there were no changes in the brain MDA and GSH levels of BPA+C, NP+C and OP+C groups compared with BPA, NP and OP treatment groups, respectively. In histopathologic examination, the vitamin C co-administrated groups had much more hyperchromatic cells in the brain cortex than that observed in the groups treated with only BPA, NP, and OP. The results of this study demonstrate that BPA, NP and OP generate reactive oxygen species that caused oxidative damage in the brain of male rats. In addition, vitamin C co-administration along with BPA, NP, and OP aggravates this oxidative damage in the brain of rats.

Carbendazim induced haematological, biochemical and histopathological changes to the liver and kidney of male rats

Carbendazim is a systemic broad-spectrum fungicide controlling a wide range of pathogens. It is also used as a preservative in paint, textile, papermaking and leather industry, as well as a preservative of fruits. In the present study, carbendazim was administered at 0, 150, 300 and 600 mg/kg per day doses orally to male rats (Rattus rattus) for 15 weeks. At the end of the experiment, blood samples, liver and kidney tissues of each animal were taken. Serum enzyme activities, and haematological and biochemical parameters were analysed. In toxicological tests, 600 mg/kg per day doses of carbendazim caused an increase of albumin, glucose, creatinine and cholesterol levels. Also, at the same doses, white blood cell and lymphocyte counts decreased. However, mean cell hemoglobin and mean cell hemoglobin concentrations increased. Histopathological examinations revealed congestion, an enlargement of the sinusoids, an increase in the number of Kupffer cells, mononuclear cell infiltration and hydropic degeneration in the liver. At the highest doses, congestion, mononuclear cell infiltration, tubular degeneration and fibrosis were observed in the kidney tissue. These results indicate that 300 and 600 mg/kg per day carbendazim affected the liver and kidney tissue and caused some changes on haematological and biochemical parameters of rats.

A Pilot Study of Heavy Metal Concentration in Various Environments and Fishes in the Upper Sakarya River Basin, Turkey

In this study, concentration of lead, cadmium, copper, cobalt, nickel, and manganese were measured in water, sediment, and fish (Cyprinus carpio and Barbus plebejus) samples at the upper Sakarya river basin in Sept. 1995–1996 period. Also, physical parameters of selected stations in the Sakarya river were measured. Mean concentrations of lead, cadmium, copper, nickel, and manganese differed between water, sediment, and fish samples by seasons. Mean concentrations of lead, cadmium, and cobalt increased in sediment samples in October and August. In water samples only cadmium and cobalt increased in October whereas lead and copper increased in August. Also, high levels of manganese concentrations were detected in water and sediment samples and fish tissue during the study. ©1999 John Wiley & Sons, Inc. Environ Toxicol 14: 367–373, 1999

Pro-oxidant effect of vitamin C coadministration with bisphenol A, nonylphenol, and octylphenol on the reproductive tract of male rats.

This study was performed to investigate whether bisphenol A (BPA), nonylphenol (NP), and octylphenol (OP) induce oxidative stress on the reproductive tract of male rats and if coadministration of vitamin C can prevent any possible oxidative stress. Wistar male rats were divided into seven groups as control (vehicle; olive oil), BPA, NP, OP, BPA+C, NP+C, and OP+C. BPA, OP, and NP groups (25 mg/kg/day) were administered orally to rats three times a week for 45 days. In BPA+C, NP+C, and OP+C groups, vitamin C (60 mg/kg/day) was administered orally along with BPA, OP, and NP (25 mg/kg/day) treatments. Malondialdehyde (MDA) appeared at significantly higher concentrations in BPA-, NP-, and OP-treated groups, when compared to control group. No significant decrease was observed in testes MDA levels of vitamin C coadministrated groups, compared with BPA, NP, and OP treatment groups. Decreased levels of reduced glutathione (GSH) were found in testes of BPA-, NP-, OP-treated rats. No significant increase was observed in testes GSH levels of BPA+C, NP+C, and OP+C groups, compared with BPA, NP, and OP treatment groups. Histological examination showed that vitamin C coadministrated groups had much more congestion areas, atrophy, and germinal cell debris in testes than those observed in other groups. Abnormal sperm percentages of BPA, BPA+C, NP+C, and OP+C groups were increased. In conclusion, the present results demonstrated that BPA, NP, and OP generate reactive oxygen species that cause oxidative damage in testes of rats. Coadministration of vitamin C aggravates this damage.

Vitamin C coadministration augments bisphenol A, nonylphenol, and octylphenol induced oxidative damage on kidney of rats

The aim of this study was to investigate whether bisphenol A (BPA), nonylphenol (NP), and octylphenol (OP) induce oxidative stress on the kidney tissue of male rats and whether coadministration of vitamin C, an antioxidant, can prevent any possible oxidative stress. The Wistar male rats were divided into seven groups, including control, BPA, NP, OP, BPA+C, NP + C, OP +C. BPA, NP, and OP (25 mg/kg/day) was administered alone; vitamin C (60 mg/kg/day) was administered along with BPA, OP, and NP to the rats for 50 days. There was a decrease in serum concentration of blood urea nitrogen (BUN) in NP and OP groups compared with control group. Vitamin C coadministration with BPA, NP, and OP did not produce significant increase in BUN concentration in BPA +C, NP+ C, and OP + C group as compared with BPA, NP, and OP groups, respectively. The lowest serum creatinine activity and the highest lactate dehydrogenase (LDH) activity was present in kidney of BPA+C, NP+C and OP+C groups compared with BPA, NP, and OP groups. The malondialdehyde (MDA) levels were significantly higher while glutathione (GSH) levels were lower in treatment groups than controls. Furthermore, an increase was observed in MDA levels whereas a decrease was observed in GSH levels in BPA+ C, NP + C, and OP+ C groups compared with BPA, NP, and OP groups, respectively. These finding are in accordance with immunohistochemical staining of MDA and GSH. Histopathological examination of the kidneys of rats in BPA, OP, NP, BPA+ C, NP + C, and OP+ C groups revealed necrotic lesions, congestion, and mononuclear cell infiltration. In conclusion BPA, NP, and OP might induce oxidative damage in kidney of rats. In addition, coadministration of vitamin C with BPA, NP, and OP to male rats augments this damage in the kidney of male rats.

Effects of carbendazim on rat thyroid, parathyroid, pituitary and adrenal glands and their hormones.

The purpose of this study is to determine the effects of low and high dose of carbendazim on the level of certain hormones and endocrine glands (thyroid, parathyroid, adrenal and pituitary glands) of male rats. Carbendazim is a systemic fungicide with activity against a number of plant pathogens. In this study, daily doses of 0, 150, 300 and 600 mg/kg per day carbendazim were applied to male rats by gavage for 15 weeks. At the end of the experiment, T3, T4, TSH, ACTH and GH levels in rat serum were analysed. Thyroid, parathyroid, adrenal and pituitary glands of rats were taken. A significant increase was observed in serum T3 levels of the rats, which were exposed to 300 mg/kg per day carbendazim doses, compared to the serum T3 levels of the control group. There were no differences between the control and carbendazim-treated group of rats regarding serum TSH, T4, ACTH and growth hormone levels. This showed us that carbendazim caused histopathological damages in thyroid, parathyroid and adrenal glands of rats. No changes were observed in pituitary glands of treated rats. These results suggest that a high quantity of subchronic carbendazim exposure affects thyroid, parathyroid and adrenal glands.

Hepatic and renal functions in growing male rats after bisphenol A and octylphenol exposure.

This study aimed to determine the effects of 13-week bisphenol A (BPA) and octylphenol (OP) exposure on the liver, kidney, and spleen of growing male rats. A total of 29 male Wistar rats aged 4–5 weeks were divided into five groups. The treatment groups were given low-dose (125 mg/kg bw/day) or high-dose (250 mg/kg bw/day) BPA or OP. These compounds were dissolved in corn oil and given via oral route for 13 weeks. Rats in the control group received corn oil for 13 weeks, as well. After 13 weeks of treatment, blood samples were analyzed for biochemical parameters. Tissue samples from the liver, kidney, and spleen were histopathologically and histomorphometrically examined. Liver tissue specimens were also stained by immunohistochemically; the number of apoptotic cells was counted, and the apoptotic indices were calculated. There were significant differences between the control and treatment groups with respect to the following parameters: body weight, relative left kidney weight, and total protein, glucose, and alkaline phosphatase levels. Edema and parenchymal degeneration in the liver and tubular degeneration in the kidney were more frequent in the treatment groups. The control and treatment groups were comparable with respect to the frequency of histopathological lesions in the spleen. Glomerular histomorphometry revealed no significant differences between the control and treatment groups. No significant differences existed between the control and treatment groups with respect to the number of apoptotic cells and apoptotic indices. Subchronic exposure to BPA and OP induced functional and structural changes in the liver, kidney, and spleen of growing male rats.

The estrogenic effects of apigenin, phloretin and myricetin based on uterotrophic assay in immature Wistar albino rats

Chemicals that occur in vegetal food and known as phytoestrogens, because of their structures similarity to estrogen, have benefits on chronic diseases. Despite this, when they are taken at high amounts, they can cause harmful effects on endocrine system of human and animals. In this study, it has been intended to determine the estrogenic potencies of phytoestrogens apigenin, phloretin and myricetin whose affinities for estrogen receptors in vitro. The female rats divided into 17 groups, each containing six rats. There was a negative control group and there were positive control dose groups which contains ethinyl estradiol, ethinyl estradiol+tamoxifen and genistein. The other dose groups which were tested for estrogenic activity contains apigenin, myricetin and phloretin All chemicals have been given to Wistar immature female rats with oral gavage for 3 consecutive days. By using uterotrophic analysis, uterus wet and blotted weights, vaginal opening, uterus length of female rats has been recorded at the end of the experiment. For detect of cell response, luminal epithelium height, gland number and lactoferrin intensity in luminal epithelium of uterus were evaluated. Biochemical analysises in blood were performed. Relative uterus weights of rats in 100 mg/kg/day dose group of myricetin were statistically increased according to vehicle control and positive control groups. In dose groups of apigenin and phloretin it was found that there were cell responses in uterus. All treatment groups had a significant difference in the high intensity of lactoferrin and uterine gland count compared to oil control group. There was no difference between phloretin and apigenin treatment groups in uterine weight statictically. Uterine heights were increased in positive control groups and 100 mg/kg/day dose group of myricetin. Epithelial cell heights were increased in treatment groups except apigenin and phloretin dose groups. There was no difference between all treatment groups in vaginal opening values according to positive control.

Influence of in utero di-n-hexyl phthalate and dicyclohexyl phthalate on fetal testicular development in rats.

This study investigated the effects of di-n-hexyl phthalate (DHP) and dicyclohexyl phthalate (DCHP) on male reproductive development in utero. Pregnant rats were exposed to DHP and DCHP at doses of 0 (vehicle), 20, 100 and 500mg/kg/day, by gavage, on gestational days (GD) 6-19. A significant decrease in the anogenital distance (AGD) of male fetuses was observed at all doses of DHP and DCHP. The AGD/cube root of body weight ratio in male fetuses was also significantly reduced compared to control group. The litters with resorption, percentage of resorptions and inhibin B levels increased in treatment groups. Moreover, testosterone and MIS/AMH levels in all treatment groups decreased. Although FSH and inhibin B levels of male pups exposed to DHP and DCHP increased, FSH/inhibin B ratio decreased in treatment groups. Reduced testosterone production in response to DHP and DCHP exposure appeared to be related to changes in testosterone metabolism, as shown by decreased 3β-HSD immunoexpression. The percentages of large Leydig clusters increased after exposure to DHP and DCHP in utero. Histopathological examination of the testis on GD20 revealed changes at all doses. Relative integrated immunodensities of 3β-HSD, MIS/AMH, PCNA and AR decreased after DHP and DCHP exposures. Altered fetal Sertoli cell development and function may be caused by disrupted PMC function revealed by reduced AR production in these cells in treatment groups.