Document Type : Original Article
Department of Biochemistry, Faculty of Vet. Med., Benha University, Egypt.
Department of Animal health, Faculty of Vet. Med., Benha University, Egypt.
Department of Biochemistry and food deficiency,Animal health research institute,Dokki, Giza, Egypt.
Department of Animal Reproduction and AI.,Veterinary Research Division, National Research Centre, Egypt.
N-acetylcysteine (NAC), as a nutritional supplement, is a greatly applied antioxidant invivo and in vitro. NAC is a precursor of L-cysteine that results in glutathione elevation biosynthesis.The therapeutic potential ofN-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 attenuatingapoptosis effect ofNACon imidaclopride (IMI) induced testicular damage in rats. Forty male albino rats wereclassified randomly into four equal groups. Group1 (control). Group2 (IMI): rats receivedIMIorally day after day over a period of 8 weeks at a dose level of 21.2mg/kg b.w (1/20 LD50). Group3 (NAC):rats received NAC(200 mg/kg body weight) orally for8 weeks.Group 4 (NAC+IMI): rats received NAC(200 mg/kg body weight) orally for 4 daysbefore 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, andDNA 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.
NACprotection to IMI induced testicular damage in rats caused a significant improvement of
all previous parameters and attenuate the histopathological changes. These results suggested that, NAC treatment exerts a protective effect on testicular damage by improving ofoxidative stress markers and DNA damage detected by comet assayin rats through free radical scavenging and anti-inflammatory activities as well as regenerating endogenous antioxidant defense system mechanisms.