Evaluation of honey protective effect on lead induced oxidative stress in rats

Lead toxicity is a worldwide health problem due to continuous exposure of the population to lead in the environment especially workers in industries. It affects many body organs especially the liver and kidneys. The aim of this study is to investigate the protective effect of natural honey against lead induced oxidative stress, hepatotoxicity and nephrotoxicity. Forty male albino rats were used in this study divided into 4 equal groups. Group [I] the control group were given distilled water orally for 4 weeks. Group [II] rats were given 1.5 ml/kg natural honey orally for 4 weeks. Group [III] rats were given lead acetate [0.2%] in drinking water for 4 weeks .Group [IV] rats were given lead acetate [0.2%] in drinking water and 1.5 ml/kg natural honey orally for 4 weeks. Blood and tissue samples were taken after four weeks. Lipid peroxidation product, malondialdehyde [MDA] in plasma, liver and kidney were determined, blood glutathione peroxidase activity [GPx] and serum nitric oxide [NO] levels were also measured, Liver function tests [serum alkaline phosphatase [ALP], aspartate transaminase [AST] and alanine transaminase[ALT] were measured. Kidney function tests [blood urea and s. creatinine] were estimated. Histopathological examination of liver and kidney sections was performed. showed significant [P>0.01] increase in the mean MDA of plasma. liver and kidney of lead acetate group [Group III] with decreased antioxidant enzyme activity [GPx] activity and [NO] and increase levels of AST, ALT, ALP, urea and serum creatinine together with histopathological changes in liver and kidney sections. Honey alleviated the increased MDA levels, and ameliorate the elevated AST, ALT, ALP, urea and serum creatinine in the combination group. The present study revealed that natural honey could diminish the adverse effects of lead acetate as shown in the histological analysis of rat livers and kidneys. The present results indicated that natural honey can modulate the damage in liver and kidney cells from oxidative stress induced by lead toxicity in tart

Vitamin A against the acetaminophen- induced toxicity in the renal cortex of albino rats

Acetaminophen [paracetamol; APAP] - induced toxicities have been a major problem in clinical practice. There is no specific treatment for paracetamol poisoning. Vitamin A has shown to have an assisting role in the management of renal inflammatory disorders in animal models as it has anti-inflammatory, antioxidant as well as cytoprotective effect on various renal cell types. To evaluate the possible protective effect of vitamin A against APAP -induced acute renal toxicity in rats. Forty adult male albino rats were used and divided into five groups including control untreated, control vitamin A [12000 IU/kg b.wt, oral], APAP [Ig/kg b.wt, intraperitoneally], APAP+ vitamin A [3000 IU/kg b.wt, oral] and APAP+ vitamin A [12000 IU/kg b.wt, oral]. One week after APAP administration, all rats were anaesthetized. Venous blood was collected; serum and plasma were separated for biochemical assessments. The kidneys were also removed and the renal specimens were submitted to biochemical analysis as well as the microscopic examination using both the light and electron microscopy. Acetaminophen treatment induced increased lipid peroxidation in the plasma and renal tissue. Additionally, increased serum BUN and creatinine levels as well as decreased antioxidant catalase activity were detected indicating a possible involvement of oxidative stress in acetaminophen-induced nephropathy. Microscopic examination revealed massive proximal tubular degeneration, luminal cellular debris associated with partial loss of the luminal brush border. Additionally, cortical interstitial vascular congestion and extravasation of red blood cells were observed. Vitamin A treatment markedly reduced paracetamol- induced renal cortical damage in a dose - dependant manner, as evidenced by the improvement of the biochemical measurements and the marked amelioration of renal pathology. Vitamin A may be a choice of preventive treatment against paracetamol- induced renal damage. The mechanism of protection is probably due to its antioxidant properties and the repairing effect on the damaged tubular cells