Metabolic fate of fenitrothion in liver, kidney and brain of rat

Abstract

The metabolic fate of fenitrothion, O,O-dimethyl-O-(3-methyl-4-nitro phenyl) phosphorothioate, was investigated in rat tissues during the first 24 hours following the intramuscular administration of the pesticide in the animal. High performance liquid chromatography (HPLC) of the pesticide and its metabolites formed in liver, kidney and brain showed the time-dependent sequential conversion of the pesticide into three major metabolites. These metabolites were separated and purified to homogeneity by HPLC and characterized by IR spectroscopy as O,O-dimethyl-O-)3-methyl-4-aminophenyl) phosphorothioate (metabolite I), O,O-dimethyl phosphorothioate (metabolite II), and O,O-dimethylphosphate (metabolite III). These results indicated reduction of the nitro group in fenitrothion aas the first step, followed by the hydrolytic cleavage of the P-O-aryl bond in metabolite I and the oxidative desulphurylation of metabolite II. Fenitrothion was found to induce ultrastructural changes in liver cells especially after 12 h exposure nuclear membrane was completely distorted, nuclear intactness was totally lost and smooth endoplasmic reticulum and Golgi apparatus were abnormally enlarged. In 24 h, however, the regeneration of the nuclear material was observed.

Effect of Refining Processes on Magnitude and Nature of Fenitrothion and Pirimiphos-Methyl Residues in Maize Oil and Bioavailability of their Cake Residues on Rats*

“…This result agrees with some previous reports (35)(36)(37) which noted that, in adult rats, the insecticide is metabolized to phosphorothioate and dimethylphosphate compounds. While compound VI represented the main substance in collected urine in free and conjugated form besidetraces of compounds VII and VIII in case of pirimiphos-methyl.…”

Modulatory effect of Turnera diffusa against testicular toxicity induced by fenitrothion and/or hexavalent chromium in rats

“…Oxidative stress is known to cause a disruption of the oxidant–antioxidant balance leading to alterations of cellular macromolecules, disturbance in cell function and eventually can lead to cell death . In addition, fenitrothion inhibits acetylcholinesterase activity, thus disrupting the nervous system and causes conformational changes in liver and kidney cells of rats with complete damage of the nuclear membrane, total loss of nuclear intactness, and abnormally enlarged smooth endoplasmic reticulum …”

Dietary supplementation with Punica and Physalis attenuates the deleterious effects of fenitrothion in rats.

“…Previous studies have shown that exposure to pesticides caused hepatotoxicity (Kalender et al, 2010), hematotoxicity (Durak et al, 2009), genotoxicity (Giri et al, 2002). In addition, OPIs can alter antioxidant enzyme activities and increase the production of free radicals in different tissues including the liver (Kumar et al, 1993); (Hazarika et al, 2003), brain (Kumar et al, 1993); (Brocardo et al, 2005) and kidney (Kumar et al, 1993); (Possamai et al, 2007).…”