Study of commonly used organophosphate pesticides that induced oxidative stress and apoptosis in peripheral blood lymphocytes of rats

Abstract

<jats:p> In a previous study, we have found that organophosphate (OP) pesticides such as chlorpyrifos (CPF), methyl parathion (MPT), and malathion (MLT) significantly induced genotoxicity in peripheral blood lymphocytes of rats. To explore the mechanism of OP-induced genotoxicity, we measured the formation of DNA interstrand cross-links (DICs) and apoptosis in peripheral blood lymphocytes of rats. Peripheral blood lymphocytes of rats were treated with CPF, MPT, and MLT individually and in combination at concentrations of 0.1 and 0.25 LC<jats:sub>50</jats:sub> for 2, 4, 8, and 12 h at 37°C. Lipid peroxidation (LPO) was measured as a biomarker of oxidative stress. Apoptosis induced by CPF, MPT, and MLT individually and in combination was determined by measuring the intracellular level of active caspase-3 and caspase-9 by spectrofluorimetry. We found significant dose- and time-dependent increases in LPO, DICs formation and increase of intracellular active caspase-3 and caspase-9 in exposed peripheral blood lymphocytes of rats. These findings suggest that the studied pesticides have potential to induce oxidative stress, cause DNA adduct formation, and cause failure of adduct repair, which leads to apoptosis that is partially mediated by activation of intracellular caspase-3 and caspase-9. </jats:p>

Ameliorative effect of nanoencapsulated flavonoid against chlorpyrifos‐induced hepatic oxidative damage and immunotoxicity in Wistar rats

“…The results of the present study (Table ) indicated that exacerbation of oxidative injury in the liver of CPF‐treated rats was more than the control group. Indeed, the involvement of oxidative stress following exposure to OP has been reported . In the present study, coadministration of NEQ in CPF‐induced toxicity has protected the liver from lipid peroxidation and from any changes in GSH and antioxidant enzymes.…”

“…Indeed, the involvement of oxidative stress following exposure to OP has been reported. [40,41] In the present study, coadministration of NEQ in CPF-induced toxicity has protected the liver from lipid peroxidation and from any changes in GSH and antioxidant enzymes. This finding explained as reported earlier the important role of natural antioxidant in preventing hydroxyl radicals' formation and in protecting the integrity and the functions of tissues.…”

Quercetin plays protective role in oxidative induced apoptotic events during chronic chlorpyrifos exposure to rats

“…Further, elevated PCC contents indicate oxidation of various proteins after CPF intoxication and that would lead to inhibition or alteration of the activities of various cellular proteins. However, simultaneous treatment with quercetin showed a decline in PCC levels that can be attributed to free radical‐scavenging property of quercetin …”

“…However, simultaneous treatment with quercetin showed a decline in PCC levels that can be attributed to free radical-scavenging property of quercetin. [26] Acetylcholinesterase activity is a standard biomarker used to study neurotoxic effects of organophosphate pesticides. Acetylcholinesterase is a membrane bound enzyme, which transforms acetylcholine into choline and acetate.…”

Effect of sodium aescinate on methyl parathion-induced myocardial injury in rats

“…Cardiac complications, such as various arrhythmias, dysarteriotony, and myocardial damage, are major causes of death after AOPP [4]. Researchers found that pesticides induce oxidative stress, causing DNA damage and apoptosis in myocardial cells; these effects may constitute the mechanism of MP-induced myocardial injury [5]. However, most research focuses on clinical treatment and lung injury, and only a few studies are aimed at understanding prevention and treatment of myocardial injury.…”