Testicular Toxicity In Adult Rats Research Articles

Histological and biochemical evaluation of the possible protective effect of thymoquinone loaded nanostructured lipid carriers versus thymoquinone on cisplatin induced testicular toxicity in adult rats.

Histological and biochemical evaluation of the possible protective effect of thymoquinone loaded nanostructured lipid carriers versus thymoquinone on cisplatin induced testicular toxicity in adult rats.

Ameliorative Effect of Nigella Sativa on Tramadol-Induced Testicular Toxicity in Adult Rats

Ameliorative Effect of Nigella Sativa on Tramadol-Induced Testicular Toxicity in Adult Rats

Beneficial Role of Ginger Powder (Zingiber officinale) against Acephate-induced Reprotoxicity in Adult Male Rats

Aims: The present study was aimed to investigate the protective role of ginger against acephate-induced testicular toxicity in adult rats.
 Methodology: Rats were allocated into four groups where animals in group I served as controls, while animals in group II, III and group IV were treated as experimental rats. Rats in groups II, III and IV were treated with acephate (50mg/kg body weight), ginger (100mg/kg body weight) and combination of both acephate and ginger, respectively over a period of 60 days. After completion of experimental period sperm count, sperm viability, sperm motility, sperm membrane integrity, testicular steroidogenic marker enzymes (3β-HSD and 17β-HSD, serum testosterone and testicular architecture was performed in both control and experimental rats.
 Results: Relative weights of reproductive organs, sperm count, sperm viability, sperm motility and sperm membrane integrity were significantly decreased in acephate treated rats over controls. Acephate administration also reduced the circulatory levels of testosterone associated with a significant reduction in the testicular steroidogenic marker enzymes (3β-HSD and 17β-HSD) in rats. The testicular architecture was disrupted in acephate intoxicated rats. In contrast, ginger administration significantly recovered the acephate-induced suppressed selected reproductive parameters with increased circulatory levels of testosterone and restoration of sperm endpoints in as compared to acephate alone treated rats. No significant changes were observed in any of the selected reproductive endpoints in ginger treated rats as compared to controls.
 Conclusion: The results can be concluded that supplementation of ginger mitigates the negative effects of acephate on male reproductive health via amelioration of testicular setroidogenesis and spermatogenesis and epididymal sperm maturation events in rats.

Induction of heme oxygenase-1 with hemin alleviates cisplatin-induced reproductive toxicity in male rats and enhances its cytotoxicity in prostate cancer cell line

Cisplatin-induced testicular damage is a major obstacle in the application of cisplatin as chemotherapeutic agent. However, it remains as one of the most widely employed anticancer agents in treating various solid tumors including prostate cancer. Since heme-oxygenase-1 (HO-1) is a cytoprotective enzyme with anti-oxidative stress, anti-inflammatory and anticancer activities, we investigated the effects of up-regulation of HO-1 by hemin and its inhibition by zinc protoporphyrin-IX (ZnPP) on cisplatin-induced testicular toxicity in adult rats. Furthermore, the anticancer effect of hemin and ZnPP, with and without cisplatin, was evaluated on human prostate cancer cell line, PC3. Results of the animal study showed that hemin reversed cisplatin-induced perturbations in sperm characteristics, normalized serum testosterone level, and ameliorated cisplatin-induced alterations in testicular and epididymal weights, and restored normal testicular architecture. Moreover, hemin increased the expression and activity of HO-1 protein and prevented cisplatin-induced testicular toxicity by virtue of its antioxidant and anti-inflammatory effects. This effect was evidenced by amelioration of testicular oxidative stress markers (malondialdehyde, nitric oxide, reduced glutathione contents, and catalase activity) and inflammatory mediators (tumor necrosis factor-α and nitric oxide synthase expressions). In contrast, administration of ZnPP (HO-1 inhibitor) did not show significant improvement against cisplatin-induced testicular toxicity. Finally, in vitro analyses showed that, hemin augmented the anticancer efficacy of cisplatin, while ZnPP inhibited its apoptotic effect in PC3 cells. In conclusion, the induction of HO-1 represents a potential therapeutic approach to protect the testicular tissue from the detrimental effects of cisplatin without repressing, but rather augmenting, its cytotoxic effects on PC3 cells.

Involvement of Neurotransmitter and Nrf2 in Nicotine- and Cigarette Smoke-Induced Testicular Toxicity in Adult Rats

Several organ systems can be affected by nicotine/cigarette smoking (CS); however, there is a gap of knowledge about the role of local neurotransmitter system, brain-derived neurotrophic factor (BDNF), and dopamine (DA) in testicular toxicity. Therefore, the aim of the present study is to explore the toxic impact of short- and long-term exposure to oral nicotine and passive CS on adult albino Wistar rats, using doses that closely mimic the human smoking scenario. Our results showed dose- and time-dependent loss of developing spermatogonia and spermatocyte of the seminiferous tubules, disruption of basement membrane, DNA damage, and high serum cotinine upon exposure to nicotine and CS, resulting in low sperm count as compared to control. Further, the results showed the upregulation of BDNF, DA, tyrosine hydroxylase (TH), and pro-oxidants, ie, reactive oxygen species (ROS) and inducible nitric oxide synthetase (iNOS), in the exposed testis and downregulation of the antioxidants such as, ascorbate and Nrf2 when compared with the control. Thus, our results for the first time highlight a potential role of the local neurotransmitter system and antioxidant depletion (Nrf2) in nicotine/CS-induced testicular pathogenesis, which could underpin the development of therapeutic interventions targeted at oxidative stress-associated disorders, and probably establish a link with the brain system contributing to addiction.

Quercetin attenuates di-(2-ethylhexyl) phthalate-induced testicular toxicity in adult rats.

The aim of the present study was to investigate the potential oxidative damage of di-(2-ethylhexyl) phthalate (DEHP) in the rat testis and to further elucidate the potential modulatory effect of quercetin. DEHP was diluted in corn oil and given to rats by oral gavage at doses 0, 300, 600, and 900 mg/kg/day (groups I, III, IV, or V, respectively) for 15 consecutive days. Group VI was pretreated with quercetin (90 mg/kg), 24 h before starting the experiment and then treated with DEHP (900 mg/kg/day) for 15 consecutive days. Group II was treated with quercetin (90 mg/kg/day). The relative testes weight and sperm motility were significantly decreased by treatment with 900 mg/kg of DEHP. Both sperm count and daily sperm production were significantly decreased by DEHP treatment at doses of 600 and 900 mg/kg. Serum testosterone level and prostatic acid phosphatase (ACP) activity and testicular lactate dehydrogenase-X (LDH-X) activity were significantly decreased in animals treated with 900 mg/kg. Serum total ACP activity was significantly increased in animals treated with 600 and 900 mg/kg of DEHP. DEHP treatment induced oxidative stress and histopathological abnormality. These abnormalities were effectively normalized by pretreatment with quercetin except for LDH-X near normalcy. In conclusion, the findings of this study demonstrate that DEHP impairs testicular function at least, in part, by inducing oxidative stress and quercetin has a potent protective effect against DEHP-induced testicular toxicity in rats.

The effect of coadministration of α-tocopherol and ascorbic acid on arsenic trioxide-induced testicular toxicity in adult rats

Arsenic, acting as an endocrine disruptor, causes reproductive malfunctions. Studies have been undertaken to find out whether the co-supplementation of α-tocopherol and ascorbic acid (AT-AA) could reduce the arsenic-induced testicular toxicity caused by oxidative stress and resulting DNA damage. Adult male Wistar rats (120±10 g) were given arsenic trioxide [3 mg/kg body weight (b.wt.) per day] for 30 consecutive days and the supplement group received α-tocopherol (400 mg/kg b.wt. per day) and ascorbic acid (200 mg/kg b.wt. per day). Reproductive functions were evaluated with respect to the histoarchitecture, gametokinetic activity, androgenic potential, glutathione-dependent antioxidant status and DNA damage of the testis. Arsenic treatment caused marked reduction in the relative weight of the testis (p<0.05) but showed no effect on body weight. The number of germ cells at stage VII of the spermatogenic cycle (p<0.01), the seminiferous tubular diameter (p<0.001) and Leydig cell nuclear area (p<0.01) were significantly reduced. Notable decrease in the activities of testicular Δ5, 3β-HSD (p<0.05) and 17β-HSD (p<0.01) with a concomitant fall in serum testosterone level (p<0.01) along with significant diminution in testicular glutathione S-transferase (p<0.05) activity and reduced glutathione level (p<0.01) were observed. Significant DNA damage (p<0.001) in spermatogenic cells was also noted. All these alterations including DNA strand breakage were seen to be protected with the coadministration of AT-AA. The data suggest that the protection of testicular toxicity in arsenic-exposed adult rats is possible with combined coadministration of AT-AA.