Ameliorative effect of tannic acid against benzo(a)pyrine-induced cytotoxicity and alterations in gene expressions in testicular tissues of rats (original) (raw)
Related papers
Effects of Benzo(a)pyrene on Intra-testicular Function in F-344 Rats
International Journal of Environmental Research and Public Health, 2008
The objective of this study was to evaluate the reproductive risk associated with exposure of adult male Fisher-344 (F-344) rats to inhaled benzo(a)pyrene (BaP), a ubiquitous environmental toxicant present in cigarette smoke, automobile exhaust fumes and industrial emissions. Rats were assigned randomly to a treatment or control group. Treatment consisted of exposure of rats via nose-only inhalation to 75μg BaP/m 3 , 4 hours daily for 60 days, while control animals were unexposed (UNC). Blood samples were collected immediately on day 60 of exposures (time 0) and subsequently at 24, 48, and 72 hours, to assess the effect of exposures to BaP on plasma testosterone and luteinizing hormone (LH) concentrations. Mean testis weight, total weight of tubules and total tubular length per paired testes were reduced 33% (P< 0.025), 27% (P < 0.01) and 39%, respectively in exposed rats (P < 0.01) compared with UNC rats. The number of homogenization-resistant spermatids was significantly reduced in BaP-exposed versus UNC rats. Plasma testosterone and intra-testicular testosterone (ITT) concentrations were significantly decreased by BaP compared with those of UNC rats. The decreases in circulating plasma testosterone were accompanied by concomitant increases in plasma LH concentrations in BaP-exposed versus control rats (P < 0.05). These data suggest that 60 days exposure to inhaled BaP contribute to reduced testicular endocrine and spermatogenic functions in exposed rats.
Journal of Genetic Engineering and Biotechnology, 2011
Exposure to chemicals like benzo(a)pyrene (BaP) can lead to structural changes in DNA and as a consequence to increased incidence of diseases with a genetic basis, as well as oxidative stress in the testis. However its ability to induce oxidative DNA damage in germ cells is not fully investigated. In the present study, BaP was used to induce 8-hydroxydeoxyguanosine (8-OHdG), a specific DNA adducts for oxidative DNA damage, in testis and epididymal sperm and the possible protection role of radish and/or cress was investigated. The results revealed that BaP induced a significant increase in DNA damage in both tissues, as indicated by increased DNA strand breaks in a fluorimetric analysis of DNA unwinding (FADU). Furthermore, it increased the oxidative damage in epididymal sperm, as indicated by the increase in sperm abnormalities, lipid peroxidation (LPO), accompanied with a decrease in glutathione content (GSH), sperm count and sperm motility as well as induction of filtration in the histology of the testis. Treatment with radish and/or cress oil prior to BaP injection succeeded in reducing the germ cell genotoxicity as indicated by the decrease in DNA damage, 8-OHdG levels, sperm abnormalities, LPO level and increased sperm counts, motility and GSH content. Moreover, cress was found to be effective than radish and the combined treatment was more effective than the single treatment. It could be concluded that, pretreatment with radish and/or cress improved the epididymal sperm quality and reduced the genotoxicity and DNA damage induced by BaP, thereby declaring the protective role of radish and cress.
Environmental science and pollution research international, 2016
Benzo[a]pyrene (B[a]P) is an environmental toxicant and endocrine disruptor. Therefore, the aim of the present study was to investigate the toxicity of B[a]P in testis of rats and also to study the role of silymarin and thymoquinone (TQ) as natural antioxidants in the alleviation of such toxicity. Data of the present study showed that levels of testosterone, estrogen and progesterone were significantly decreased after treatment of rats with B[a]P. In addition, B[a]P caused downregulation of the expressions of steroidogenic enzymes including CYP17A1 and CP19A1, and decreased the activity of 17-β hydroxysteroid dehydrogenase (17β-HSD). Moreover, B[a]P decreased the activities of antioxidant enzymes including catalase (CAT), glutathione peroxidase (GPX) and superoxide dismutase (SOD), and significantly increased free radicals levels in testis of male rats. However, pretreatment of rats with silymarin prior to administration of B[a]P was found to restore the level of free radicals, anti...
BMC Genomics, 2010
Background Benzo [a]pyrene (B[a]P) exposure induces DNA adducts at all stages of spermatogenesis and in testis, and removal of these lesions is less efficient in nucleotide excision repair deficient Xpc -/- mice than in wild type mice. In this study, we investigated by using microarray technology whether compromised DNA repair in Xpc -/- mice may lead to a transcriptional reaction of the testis to cope with increased levels of B[a]P induced DNA damage. Results Two-Way ANOVA revealed only 4 genes differentially expressed between wild type and Xpc -/- mice, and 984 genes between testes of B[a]P treated and untreated mice irrespective of the mouse genotype. However, the level in which these B[a]P regulated genes are expressed differs between Wt and Xpc -/- mice (p = 0.000000141), and were predominantly involved in the regulation of cell cycle, translation, chromatin structure and spermatogenesis, indicating a general stress response. In addition, analysis of cell cycle phase dependent ...
Mutagenesis, 2010
Exposure to genotoxins may compromise DNA integrity in male reproductive cells, putting future progeny at risk for developmental defects and diseases. To study the usefulness of sperm DNA damage as a biomarker for genotoxic exposure, we have investigated cellular and molecular changes induced by benzo[a]pyrene (B[a]P) in human sperm in vitro, and results have been compared for smokers and non-smokers. Sperm DNA obtained from five smokers was indeed more fragmented than sperm of six non-smokers (mean % Tail DNA 26.5 and 48.8, respectively), as assessed by the alkaline comet assay (P < 0.05). B[a]P-related DNA adducts were detected at increased levels in smokers as determined by immunostaining. Direct exposure of mature sperm cells to B[a]P (10 or 25 mM) caused moderate increases in DNA fragmentation which was independent of addition of human liver S9 mix for enzymatic activation of B[a]P, suggesting some unknown metabolism of B[a]P in ejaculates. In vitro exposure of samples to various doses of B[a]P (with or without S9) did not reveal any significant differences in sensitivity to DNA fragmentation between smokers and non-smokers. Incubations with the proximate metabolite benzo[a]pyrener-7,t-8-dihydrodiol-t9,10-epoxide (BPDE) produced DNA fragmentation in a dose-dependent manner (20 or 50 mM), but only when formamidopyrimidine DNA glycosylase treatment was included in the comet assay. These levels of DNA fragmentation were, however, low in relation to very high amounts of BPDE-DNA adducts as measured with 32 P postlabelling. We conclude that sperm DNA damage may be useful as a biomarker of direct exposure of sperm using the comet assay adapted to sperm, and as such the method may be applicable to cohort studies. Although the sensitivity is relatively low, DNA damage induced in earlier stages of spermatogenesis may be detected with higher efficiencies.
Toxicology, 2012
Although benzo[a]pyrene (BaP) is an environmental endocrine disrupter, it has been unclear whether neonatal exposure to BaP affects the testosterone level and, if so, whether this influence persists into adulthood. In this present study, we gave neonatal rats (through oral gavages) doses of 0, 5, 10, or 25 mg/kg day of BaP in corn oil from postnatal day 1 (PND 1) to PND 7. The rats were sacrificed at PND 8, PND 35, and PND 90. BaP exposure was confirmed through the induction of liver and testis CYP1A1 mRNA expression at PND 8 (i.e., immediately after exposure). The testicular daily sperm production and the sperm counts of the epididymis cauda at PND 90 were significantly lower than those of the control. The serum testosterone levels decreased markedly at PND 8, PND 35, and PND 90 after neonatal BaP exposure relative to those of the control. The mRNA expressions of StAR also decreased relative to those of the control at PND 8, PND 35, and PND 90, although the mRNA expressions of P450c17 and 17ˇ-HSD were suppressed significantly only at PND 8. To further elucidate the mechanism of the persistent decrease in the mRNA expression of StAR, we determined the histone acetylation level in the StAR promoter. The extent of acetylation of H3K14 in the determined region decreased after neonatal exposure to BaP; this phenomenon persisted to the adult stage. Our results indicate that neonatal exposure to BaP damages testosterone production and sperm counts in the long term, possibly as a result of epigenetic regulation in the StAR promoter region.
Environmental Toxicology, 2013
The objective of this study was to assess whether subchronic exposure to benzo(a)pyrene (BaP) via oral ingestion alter endpoints of the reproductive system of mice. Hsd: ICR (CD1) 10-week-old males (n 5 8) were randomly assigned to the exposure group and control group. Mice were administered BaP for 30 and 60 days by daily gavage at doses of 1, 10, 50, and 100 mg/kg body weight per day. At the end of the experiments, mice were anesthetized and reproductive organs, including testes, seminal vesicles, prostate, and cauda epididymis, were removed and examined. Spermatozoa quality and DNA strand breaks were assessed-1 and 10 mg/kg/day of BaP for 30 and 60 days did not significantly induce altered morphology or weights of testes, prostate, seminal vesicle, and epididymis, and spermatozoa quality of mice; 100 mg/kg/day of BaP for 60 days decreased weights of testes, seminal vesicle, and cauda epididymis. BaP exposure also significantly decreased motility, normal head morphology, vitality, and concentration of mature spermatozoa. In addition, BaP exposure induced a significant increase in DNA strand breaks.