Metabolic Energy Insufficiency in Mice Kidney following Short-term Exposure to Lead: An In-vivo Study

Abstract

Background: Metabolic stress is one of the risk factors of lead-induced functional abnormalities of the tissue. The present study aims
at determining the effect of lead on certain energy metabolic profiles in renal tissue of mice.
Method: Swiss albino mice were exposed to Pb by gavages at a 5mg/kg body weight dose for 30 days. After treatment, urinary glucose,
glucose 6-phosphatase, lactate dehydrogenase, TCA cycle enzymes, different proteolytic enzyme activities, total, acidic, basic and neutral
proteins, protein carbonyl content, glyceraldehyde 3-phosphate dehydrogenase activity, tissue Pb deposition and renal morphology
were examined.
Results: Lead exposure resulted in glycosuria and decreased glucose 6-phosphatase activity in the kidney, whereas the lactate
dehydrogenase activity was increased in that tissue. The malate dehydrogenase and succinate dehydrogenase activities were stimulated
by Pb, whereas the glyceraldehyde 3-phosphate dehydrogenase activity was inhibited. Degradation of tissue protein was accompanied
with enhanced protein carbonylation. Significant changes in trypsin, cathepsin and pronase activities were noted. Decreased amino
acid nitrogen in kidney was associated with altered transaminase activity. Additionally, fatty infiltration was observed in association
with accumulation of elemental lead.
Conclusion: It is suggested that sub-acute Pb exposure modulated certain enzymes and intermediates of major energy metabolism
pathways in the renal tissue of mice to establish an adaptive mechanism against metabolic distress.