An impurity of malathion alters the morphology of rat lung bronchiolar epithelium

Imamura, Toshiko; Gandy, Joan; Fukuto, T. R.; Talbot, P A

doi:10.1016/0300-483x(83)90058-6

Cited by 40 publications

(3 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, malathion also contains toxic impurities, such as O,S,S-trimethyl phosphorodithioate (OSS). Toxicity following oral exposure to OSS in rats presents with increased levels of lactate dehydrogenase (LDH) levels, a cytotoxic marker, and altered pulmonary morphologies resulting in decreased numbers of Clara cells in the bronchial epithelium and destruction of type I pneumocytes (Imamura et al, 1983;Konno et al, 1984). Malathion itself has been shown to produce oxidative damage in the lungs of exposed rats (Possamai et al, 2007).…”

Section: Malathionmentioning

confidence: 99%

Pulmonary Mast Cells

Katwa¹,

Brown²

2015

Comparative Biology of the Normal Lung

View full text Add to dashboard Cite

Section: Malathionmentioning

confidence: 99%

Pulmonary Mast Cells

Katwa¹,

Brown²

2015

Comparative Biology of the Normal Lung

View full text Add to dashboard Cite

“…However, malathion-induced pulmonary toxicity involves severe inflammation, fibrosis and thickening of the interalveolar septa, as well as hyperemia in the blood vessels [11]. Malathion also causes changes in the respiratory tract epithelium, including a decrease in the number of Clara cells [12]. Malathion toxicity is due to various mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Estradiol and ascorbic acid alleviate malathion-induced lung damage in albino Wistar rats: A histopathological study

Alhilal,

Mohamed Salem

2024

j-ebr

View full text Add to dashboard Cite

To assess the modulatory role of estradiol and ascorbic acid in malathion-induced pulmonary toxicity in albino Wistar rats. Methods: A total of twenty albino Wistar rats were randomly divided into four groups; the control group (group 1) was given corn oil alone, the test group (group 2) received a daily dose of malathion 20 mg/kg in corn oil, treatment group A (group 3) was administered a daily dose of malathion 20 mg/kg in corn oil plus estradiol 40 µg/100 g (gram), and treatment group B (group 4) received a daily dose of malathion 20 mg/kg in corn oil plus ascorbic acid 100 mg/kg. Experimental rats were administered once daily for four weeks. The lungs were examined histopathologically using two staining methods (Hematoxylin and Eosin, Masson Trichrome). Results: There were significant reductions in degeneration, interstitial pneumonia and interstitial fibrosis for group 3 (treatment group A) compared to group 2 (test group) (p<0.05). These reductions were more statistically significant for group 4 (treatment group B) compared to group 2 (test group) (p<0.01). Therefore, the damage was less pronounced and injury severity was moderate in group 3 treated with estradiol. Group 4, with ascorbic acid, showed the most improvement with significant tissue repair under microscopic examination and mild injury compared to group 3. Conclusions:The results of our present study suggest that both estradiol and ascorbic acid have clear protective effects against malathion-induced lung injury. However, ascorbic acid exhibited more pronounced protective effects compared to estradiol. With more comprehensive studies, the positive effects of ascorbic acid and estradiol can be used to prevent lung damage in individuals exposed to malathion.

show abstract

“…O,O,S-trimethyl phosphorothioate (00s-TMP) caused lung injury in rats and mice (Verschoyle et al 1980;Dinsdale et al 1982;Verschoyle & Cabral 1982;Imamura et al 1983). Studies on the mechanism of lung injury have shown that the ultimate toxicant is an activated intermediated metabolite but not the parent compound.…”

mentioning

confidence: 99%

Enhanced Levels of Lipid Peroxidation and Xanthine Oxidase Activity in the Lung of Male Sprague‐Dawley Rats Following Treatment with O,O,S‐Trimethyl Phosphorothioate

Ohtaka

1994

Pharmacology & Toxicology

View full text Add to dashboard Cite

The purpose of this study was to investigate the roles of lipid peroxidation and a prototypical radical generating enzyme, xanthine oxidase, in lung injury caused by O,O,S-trimethyl phosphorothioate (OOS-TMP). Animals (five per group) were dosed with OOS-TMP at 40 mg/kg and sacrificed on the 1st, 3rd or 7th day after treatment. OOS-TMP increased lipid peroxidation (Mean +/- S.E.) to 139 +/- 9.6% of the control values in the lung and to 623 +/- 203% in the liver on the 1st day. When rats were dosed with OOS-TMP at 20, 40 and 60 mg/kg, lipid peroxidation in the lung and the liver were increased in a dose-dependent manner. In the lung, the total activity of xanthine oxidase was coincidentally increased. In contrast, the activities of superoxide dismutase and catalase were not affected. Effects of OOS-TMP on lipid peroxidation and the total activity of xanthine oxidase were completely abolished by coadministration with O,O,O-trimethyl phosphorothionate of a non-toxic dose (1 mg/kg), which antagonizes the lung injury after treatment with OOS-TMP. The present results indicate that free radical formation may be involved in lung injury after OOS-TMP treatment through activation of radical producing enzymes such as xanthine oxidase.

show abstract

An impurity of malathion alters the morphology of rat lung bronchiolar epithelium

Cited by 40 publications

References 7 publications

Pulmonary Mast Cells

Pulmonary Mast Cells

Estradiol and ascorbic acid alleviate malathion-induced lung damage in albino Wistar rats: A histopathological study

Enhanced Levels of Lipid Peroxidation and Xanthine Oxidase Activity in the Lung of Male Sprague‐Dawley Rats Following Treatment with O,O,S‐Trimethyl Phosphorothioate

Contact Info

Product

Resources

About