ABSTRACT
Mercuric chloride is a known human and animal nephrotoxicant. This study was conducted to evaluate the effect of N-acetylcysteine and garlic against acute and chronic nephrotoxicity induced by mercuric chloride in adult albino rats. The study included 140 adult albino rats for studying the acute and chronic toxicities of mercuric chloride. The acute toxicity study included 7 subgroups [each subgroup contains 10 rats]: subgroup I [negative control], subgroup II[positive control]:Each rat orally received 1-mLsaline in a single dose, subgroup IJI orally received mercuric chloride in a dose of 13mg/ kg body weight [1/2 Lethal Dose] in 1-mL saline as a single dose, subgroup IV [Nacetylcysteine subgroup] orally received 505mg/ kg body weight [1/10 LD[50]] in 1-mL saline, subgroup V [garlic- treated subgroup] given orally garlic in a dose of 54 mg/100 gm of body weight dissolved in 1-mL saline once daily, subgroup VI: is given mercuric chloride and N-acetylcysteine with the previous doses and subgroup VII is given mercuric chloride and garlic with the previous doses. After 24 hours urine was collected from the rats of each group to measure urinary mercuric chloride level. The rats were then sacrificed and blood samples were collected for measuring serum creatinine level. Kidney samples were subjected for histopathological examination by light microscope. The chronic mercury toxicity study included 7 Subgroups each contained 10 rats The 1[st] subgroup [negative control], 2[nd] subgroup [positive control]:Each rat orally received 1-mLsaline daily, 3[rd] subgroup orally received mercuric chloride in a dose of 2.59 mg/ kg body weight [1/10 Lethal Dose] in 1-mLsaline for each rat daily, 4th subgroup [N-acetylcysteine subgroup] orally received 505mg/ kg body weight [1/10 LD[50]] in 1-mLsaline daily, 5[th] subgroup [garlic- treated subgroup] orally given garlic in a dose of 54 mg/100 gm of body weight dissolved in 1 mL saline once daily. 6[th] subgroup given mercuric chloride and N-acetylcysteine with the previous doses and 7[th] subgroup given mercuric chloride and garlic in the previous doses all subgroups were treated for 2 months then blood samples were collected for measuring serum creatinine level then rats were sacrificed and kidney samples were taken for histopathological examination by light microscope. After 24 hours urinary mercuric chloride level was highly significantly increased in rats acutely intoxicated with mercuric chloride as compared with positive control subgroup [P < 0.001]. At the same time urinary mercuric chloride level was highly significantly increased in rats received N-acetylcysteine or garlic concomitantly with mercuric-chloride than rats received mercuric chloride alone [P < 0.001]. Serum creatinine level was highly significantly increased in rats acutely intoxicated with mercuric chloride than other groups [P < 0.001]. Histopathological findings after 24 hours in the acute toxicity study were cloudy swelling of convoluted tubular epithelium with cell necrosis. After 2 months of chronic toxicity there was a very high significant increase in serum creatinine level of the mercury intoxicated rats alone [3[rd] subgroup] when compared with rats of other subgroups [P < 0.001] and the histopathological findings were coagulative necrosis, cystic dilatation of some renal tubules, hyaline and cellular casts, thickening of Bowman's capsule with interstitial aggregation of lymphocytes. It can be concluded that. N-acetylcysteine and garlic can protect the kidney from the nephrotoxicity of mercuric chloride when concomitantly administered with it
ABSTRACT
Acute toxicity of paracetamol is associated with extensive liver damage. This study was undertaken to investigate the hepatoprotective effect of cinnamon bark oil [CBO], Nigella sativa seed oil and N-acetylcysteine [NAC] in adult male albino rats acutely intoxicated with toxic dose of paracetamol [PCM]. The study included 42 adult male albino rats divided into 7 groups each group consisted of 6 rats: negative control group receiving nothing, Saline control group receiving 2 ml saline orally. Oil control group receiving 2-ml corn oil orally. Paracetamol group receiving toxic dose of PCM 400-mg/ kg in saline orally. Three groups intoxicated first by the previous toxic dose of PCM then received the following antidotes orally respectively 2 hours later: NAC, 800 mg/kg in saline; CBO, 300 mg/ kg in corn oil and NSO, 2.88 ml/kg in corn oil. Twenty-four hours after treatment the rats were sacrificed and blood samples were collected for measuring aminotransferases [ALT and AST]. Small sample from the liver of each rat was sent for histopathological examination, the remaining part of the liver of each rat was sent for determination of the following antioxidants: glutathione [GSH], GSH- peroxidase [GSHPX], GSH reductase [GSW R] and superoxide dismutase [SOD]. The three antidotes reduced the activity of ALT and AST significantly compared to the rats received the toxic dose of PCM- alone. Liver architecture showed improvement in the antidote treated groups compared to the PCM- alone intoxicated rats. The antidotes enhanced the elevation of the antioxidant levels compared to their level in the PCM- alone treated rats. It can be concluded that CBO and NSO can protected the liver from the hepatotoxic effect of PCM as well as that of NAC