N-acetylcysteine (NAC), as a nutritional supplement, is a greatly applied antioxidant in vivo and in vitro. NAC is a precursor of L-cysteine that results in glutathione elevation biosynthesis. The therapeutic potential of N-acetylcysteine (NAC) has been investigated as a bioprotective agent against oxidative stress and ischemic injury. Also, it is used as a treatment for certain mental and physical illnesses. The aim of this study was to evaluate the protective and attenuating apoptosis effect of NAC on imidaclopride (IMI) induced testicular damage in rats. Forty male albino rats were classified randomly into four equal groups. Group1 (control). Group2 (IMI): rats received IMI orally day after day over a period of 8 weeks at a dose level of 21.2 mg/kg b.w (1/20 LD50). Group3 (NAC): rats received NAC (200 mg/kg body weight) orally for 8 weeks. Group 4 (NAC+IMI): rats received NAC (200 mg/kg body weight) orally for 4 days before and along with the administration of (IMI) over a period of 8 weeks. At the end of the experiment testes were isolated for the determination of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), reduced Glutathione (GSH) and comet assay. Also, for histopathological examination.The obtained results showed a significant increase in testicular tissue MDA, and DNA damage detected by comet assay in imidaclopride intoxicated rats. However, Testicular SOD activity, catalase, and GSH concentration were markedly decreased. Histopathological alteration caused by IMI toxicity were presented by slightly thickened tunica albuginea with less congestion of sub-capsular blood vessels, mild degeneration of the germinal epithelium of some seminiferous tubules with mild interstitial edema.NAC protection to IMI induced testicular damage in rats caused a significant improvement of
Medicinal plants have played a vital role in treatment of variety of male reproductive system disorders. Thymoquinone (TQ), is the main active components of Nigella sativa, exhibited very useful biomedical effects such as anti-inflammatory, antioxidant, antimicrobial, antiparasitic, anticancer and hypoglycemic effects. The aim of this study was to evaluate the probable protective effect of thymoquinone (TQ) on imidaclopride (IMI) induced testicular damage in rats. Forty male albino rats were classified randomly into four equal groups. Group1 (control). Group2 (IMI): rats received IMI orally day after day over a period of 8 weeks at a dose level of 21.2 mg/kg b.w (1/20 LD50). Group3 (TQ): rats received TQ orally once per day at a dose of 10 mg/kg body weight/day for 8 weeks. Group 4 (TQ+IMI): rats received TQ (10 mg/kg body weight) orally for 4 days before and along with the administration of (IMI) over a period of 8 weeks. At the end of the experiment blood samples were collected for testosterone and estradiol (E2) hormones determination, semen samples for sperm characteristics evaluation and testes for the determination of MDA, SOD, CAT, GSH and also, for histopathological examination. The obtained results reported the endocrine disruption effect of IMI resembled in marked decline in testosterone hormone, while E2 was markedly elevated. At the same time there was an insignificant reduction at sperm characteristics (motility, viability and count), while there was a highly significance elevation at sperm abnormality. Oxidative stress results showed a significant increase in testicular tissue MDA in imidaclopride intoxicated rats. However, testicular SOD activity, catalase, and GSH concentration were markedly decreased. TQ protection to IMI induced testicular toxicity in rats caused a significant improvement of all previous parameters. These results suggested possible protective role of thymoquinone to improve testicular damage by attenuating the endocrine disruptor effect of IMI on some reproductive hormones, sperm characteristics alterations or oxidative stress markers in rats through its antiinflammatory activities and free radical scavenging properties.
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