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Impaired Energy Metabolism after Co‐Exposure to Leadand Ethanol
Author(s) -
Verma Suresh Kumar,
Dua Raina,
Gill Kiran Dip
Publication year - 2005
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/j.1742-7843.2005.pto_96611.x
Subject(s) - ethanol , neurotoxicity , toxicity , mitochondrion , respiration , chemistry , alcohol dehydrogenase , metabolism , cytochrome c oxidase , biochemistry , succinate dehydrogenase , medicine , pharmacology , endocrinology , biology , anatomy , organic chemistry
The neurotoxic effects of lead are controlled by a number of nutritional, physiological and environmental factors. One such factor, ethanol, might affect the neurotoxicity of lead by regulating its absorption and distribution. However, there is little information regarding the possible biochemical mechanism by which ethanol might be affecting the state of neuronal functions in lead‐exposed individuals. Therefore, the present investigation involved the effect of alcohol (3 g/kg body weight, intragastrically, for 8 weeks) on lead‐induced (50 mg/kg body weight, intragastrically, for 8 weeks) mitochondrial dysfunction in adult rat brain. Ethanol was found to enhance the toxic effects of lead in terms of decreased cellular energy reserves (ATP levels). Co‐exposure to lead and ethanol caused marked decline in the rate of mitochondrial respiration as compared to lead alone. Further the activies of various components of the electron transport chain, viz. NADH dehydrogenase, succinate dehydrogenase and cytochrome oxidase depicted a significant decrease in the lead and ethanol co‐exposed rats as compared to the lead‐treated group. The results of the present study reflect that ethanol makes adult rat brain more vulnerable to the neurotoxic effects of lead in terms of altered mitochondrial energy metabolism.