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Oxidative stress after acute and sub-chronic malathion intoxication in Wistar rats
F P Possamai1, J J Fortunato, G Feier
1Laboratório de Fisiopatologia Experimental, Universidade do Extremo Sul Catarinense, CEP 88806-000, Criciúma, SC, Brazil.
Abstract:
Malathion is an insecticide of the group of organophosphate pesticides (OPs), which shows strong insecticidal effects. However, it possesses mutagenic and carcinogenic properties and shows organ-specific toxicity in relation to the heart, kidney and other vertebrate organs. The exact mechanism of the genotoxic effects of malathion is not yet known. Free radical damage is an important direct or indirect factor in several pathological and toxicological processes, including malathion poisoning. The aim of the present study was the evaluation of oxidative damage in different tissues of Wistar rats, administered intra peritoneally at doses of 25, 50, 100 and 150mgmalathion/kg, after acute and sub-chronic malathion exposure. Oxidative stress evaluation was based on lipid peroxidation by levels of thiobarbituric acid reactive substances (TBARS), protein oxidation by levels of carbonyl groups, and also on the activities of superoxide dismutase and catalase, two antioxidant enzymes that detoxity superoxide radical (O(2)(-)) and hydrogen peroxide, respectively. The results showed that the most sensitive targets of oxidative damage were kidney, lung and diaphragm after acute treatment, and liver, quadriceps and serum after sub-chronic treatment. Also, in general, increased lipid peroxidation measured as TBARS levels seems to be a better biomarker of oxidative stress compared to the contents of protein carbonyls after acute and sub-chronic malathion treatments. The present findings reinforce the concept that oxidative stress and particularly lipoperoxidation, are involved in OPs toxicity.
Insights
Malathion exposure causes oxidative stress, damaging organs like the kidney and liver. Lipid peroxidation is a key indicator of this damage in rats.
Area of Science:
- Toxicology
- Environmental Health
- Biochemistry
Background:
- Malathion, an organophosphate pesticide, exhibits potent insecticidal properties.
- Despite its efficacy, malathion is associated with mutagenic, carcinogenic, and organ-specific toxicity (heart, kidney).
- The precise mechanisms underlying malathion's genotoxic effects remain unclear, though free radical damage is implicated.
Purpose of the Study:
- To investigate the extent of oxidative damage in various tissues of Wistar rats following acute and sub-chronic exposure to malathion.
- To assess the role of oxidative stress and lipid peroxidation in malathion toxicity.
Main Methods:
- Wistar rats were administered malathion intraperitoneally at doses of 25, 50, 100, and 150 mg/kg.
- Oxidative stress was evaluated by measuring lipid peroxidation (TBARS levels) and protein oxidation (carbonyl groups).
- Activities of antioxidant enzymes, superoxide dismutase (SOD) and catalase, were assessed.
Main Results:
- Acute malathion exposure primarily induced oxidative damage in the kidney, lung, and diaphragm.
- Sub-chronic exposure showed significant oxidative damage in the liver, quadriceps, and serum.
- Increased TBARS levels, indicating lipid peroxidation, served as a more sensitive biomarker of oxidative stress than protein carbonyls.
Conclusions:
- Oxidative stress, particularly lipid peroxidation, plays a significant role in the toxicity of organophosphate pesticides like malathion.
- The study identifies specific organs susceptible to malathion-induced oxidative damage under different exposure durations.
- Lipid peroxidation is highlighted as a reliable biomarker for assessing malathion-induced oxidative stress.
