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Zinc reverses malathion-induced impairment in antioxidant defenses

Jeferson L Franco1, Thais Posser, Jacó J Mattos

  • 1Departamento de Ciências Fisiológicas, Centro de Ciências Biológicas, Universidade Federal de Santa Catarina, Florianópolis, SC 88040-900, Brazil.

Toxicology Letters
|May 12, 2009
PubMed

Insights

Zinc supplementation protected rats against malathion toxicity by restoring antioxidant enzyme activity. This study highlights zinc

Area of Science:

  • Neuroscience
  • Toxicology
  • Biochemistry

Background:

  • Malathion toxicity involves acetylcholinesterase inhibition and oxidative stress.
  • Zinc exhibits neuroprotective properties in various studies.
  • Understanding malathion's non-cholinergic effects and zinc's counteracting mechanisms is crucial.

Purpose of the Study:

  • To investigate the neuroprotective effects of zinc chloride against acute malathion toxicity in rats.
  • To examine malathion's impact on hippocampal acetylcholinesterase and antioxidant enzymes.
  • To explore zinc's influence on heat shock protein expression.

Main Methods:

  • Adult male Wistar rats were treated with zinc chloride for 30 days.
  • Acute malathion exposure was administered (250mg/kg, i.p.).
  • Hippocampal acetylcholinesterase activity, antioxidant enzyme levels, and heat shock protein expression (HSP60, HSP70) were measured.

Main Results:

  • Malathion significantly decreased hippocampal acetylcholinesterase and key antioxidant enzyme activities.
  • Zinc pretreatment fully restored antioxidant enzyme activity but only partially improved acetylcholinesterase levels.
  • Zinc administration increased HSP60 expression, suggesting a novel protective pathway.

Conclusions:

  • Inhibition of antioxidant enzymes is a significant non-cholinergic effect of malathion.
  • Oral zinc treatment can effectively rescue these compromised antioxidant defenses.
  • Zinc's neuroprotective action may involve preserving antioxidant capacity and inducing HSP60.

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