Lead (Pb), a threat to protein metabolic efficacy of liver, kidney and muscle in mice

Lead, being the most dangerous natural heavy metal imposes metabolic dysfunction in organ system. However, the effect of lead on protein metabolic efficacy in the liver, kidney and skeletal muscle in mice has not been well studied. The aim of the present study is to establish the metabolic orientation between the liver, kidney and muscle upon sub-acute lead exposure to assess how protein and amino acid metabolisms are affected. Lead acetate was administered by gavage at a dose of 5 mg/kg b.w./once daily for 30 days. After the treatment, the liver, kidney and muscle were evaluated for biochemical parameters such as proteolytic enzyme activities (trypsin, cathepsin and pronase), tissue protein content (acidic, basic, neutral and total protein), protein carbonyl content, free amino nitrogen as well as tissue and serum transaminase activities. Degradation of total protein was noted in the liver and kidney possibly due to enhanced carbonylation of proteins whereas it was elevated in skeletal muscle. The proteolytic enzyme activity was inhibited in the liver and elevated in the kidney by lead treatment. Muscular cathepsin and trypsin activities decreased but the pronase activity enhanced following lead exposure. Moreover, a marked reduction of transaminase enzyme activities in all the tissues might be due to enzyme leakage from tissue to blood. Significant alteration in amino acid nitrogen in the affected tissue indicates adaptive mechanisms at play in the organ system. Lead is found to be responsible for alteration of tissue protein and amino acids in a toxic fashion and promotes a cooperative mechanism to minimize the metabolic distress imposed by lead.