Attenuating Effect of N-Acetylcysteine onApoptosis Associated with ImidaclopridInduced Testicular Damage inMale Albino Rats

Abstract

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

Protective effect of acetylcysteine against thiamethoxam-induced hepatic and renal toxicity in rats

“…pesticides) [90]. In line with our obtained results A Hussein, et al [91] and Abd-Elhakim, et al [92] observed an increase in the levels of MDA in imidacloprid intoxicated rats. Also, mice intoxicated with 30 mg/kg b.w./day of thiamethoxam for 28 days showed increase in the oxidative stress parameters such as MDA level in association with decrease in total antioxidants level [15].…”

“…Otherwise, Tope and Panemangalore [18] discovered no differences in urine 8-OH-2DG levels between pesticide sprayers but detected higher levels in their plasma 8-OH-2DG samples when compared to the control. Also, A Hussein, et al [91] showed a significant increase in DNA damage detected by comet assay in imidacloprid intoxicated rats. Another study of MX-exposed zebrafish showed induction of oxidative stress and DNA damage which can be detected by the comet assay.…”

“…Also, NAC improves the viability of human hepatocytes and protects the liver [21] and kidneys [22] against oxidant damage. NAC has an ameliorative effect against many pesticides toxicity such as organophosphate compounds (Yurumez et al, 2007; [23][24][25], alpha-cypermethrin [26], carbamates [27], and imidacloprid [28]. Accordingly, the present study was aimed to investigate the protective effect of NAC on hepato-nephro-toxicity induced by MX in male rats.…”

Gracilaria edulis exhibit antiproliferative activity against human lung adenocarcinoma cell line A549 without causing adverse toxic effect in vitro and in vivo

“…A MTT assay was performed to assess the cytotoxicity of GEEA extract against the lung cancer cell line A549. The cytotoxicity of various concentrations (20,40,60, 80 and 100 µg mL −1 ) of extract was assessed at different time points (12,18,24 and 48 h). The IC 50 value for the GEEA extract was calculated using EPA Probit analysis programme v1.5.…”

“…The recent statistical reports reveal that lung cancer (85% of which is Non-small Cell Lung cancer (NSCLC)) is the second leading cause of death in the United States, Egypt and all other parts of the world. 12,26 In general, NSCLC is incurable because it develops acquired resistance after an initial response of chemotherapy and also develops intrinsic resistance to chemotherapy. 26 Currently, the discovering of potent bioactive agents is very much necessary to inhibit cell growth, target multiple signalling pathways and also to induce apoptosis.…”