Improvement of Renal Oxidative Stress and Function in Lead Acetate-Induced Renal Toxicity in Rats Followed by Ascorbic Acid Consumption

Lead is a heavy metal that causes toxicity in various tissues, including kidneys. The aim of this study was to evaluate the protective effects of ascorbic acid on lead-induced renal toxicity.

24 rats were divided into three groups: 1- Control group that consumed normal water, 2- Lead acetate group (mg/liter 500) in drinking water and 3- Lead acetate + Ascorbic acid group (1 gr/liter). After 8 weeks, the rats were completely anesthetized and blood and kidney tissues were collected.

Lead acetate caused increase in BUN and creatinine compared to control group. In addition, in Lead acetate group malondialdehyde (MDA) was elevated and glutathione (GSH) was decreased in renal tissues. In Lead acetate + Ascorbic acid group, MDA was decreased and GSH was increased in contrast to Lead acetate group.

According to this data, oral ascorbic acid consumption reduces the renal functional injury and oxidative stress following lead toxicity.