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Parathion induces mouse germ cells apoptosis
E Bustos-Obregón1, O Díaz, C Sobarzo
1Laboratory of Biology of Reproduction, Program of Morphology, University of Chile Medical School Santiago. ebustos@machi.med.uchile.cl
Abstract:
Germ cell loss occurs in normal spermatogenesis at defined stages of the seminiferous epithelial cycle. The process has been known for over a century but only recently it was analyzed under the concept of apoptosis. This is a programmed cell death that occurs during development and also in the adult. It is believed to play a key role as quality control in sperm formation, avoiding the passage of genetic defects to future generations. Chemical toxicants may increase apoptosis, disturbing tissue homeostasis. The effect of the agropesticide parathion upon apoptosis in mouse seminiferous tubules was analyzed in young mice (onset of spermatogenesis) and in adult animals (full spermatogenesis). In both young and adult mice, the pesticide increases the rate of apoptosis, which takes place at stages where spermatogonial proliferation occurs, affects spermatocytes at the beginning of the meiotic process and spermatids at the elongating period. Basal apoptotic rates are greater in young mice. In adults, commercial parathion is more toxic than the pure organophosphoric compound. From these observations plus in vitro effects of parathion reported previously, it can be concluded that the pesticide affects DNA (and RNA and protein) synthesis. The effect is reversible with moderate doses of the chemical after acute intoxication.
Insights
The agropesticide parathion increases programmed cell death (apoptosis) in mouse testes, impacting sperm formation. This effect is dose-dependent and reversible, suggesting potential for recovery after exposure.
Area of Science:
- Reproductive Biology
- Toxicology
- Cell Biology
Background:
- Germ cell loss is a normal part of spermatogenesis, crucial for genetic quality control.
- Apoptosis, or programmed cell death, is increasingly recognized as the mechanism behind this germ cell loss.
- Chemical toxicants can disrupt testicular homeostasis by increasing apoptosis.
Purpose of the Study:
- To investigate the impact of the agropesticide parathion on apoptosis in mouse seminiferous tubules.
- To compare the effects of parathion on apoptosis in mice at different stages of spermatogenesis (young vs. adult).
Main Methods:
- Analysis of apoptosis rates in seminiferous tubules of young and adult mice exposed to parathion.
- Comparison of toxicity between commercial parathion and the pure compound in adult mice.
Main Results:
- Parathion significantly increased apoptosis in both young and adult mice.
- Apoptosis occurred at specific stages: spermatogonial proliferation, meiotic initiation, and spermatid elongation.
- Basal apoptotic rates were higher in young mice.
- Commercial parathion exhibited greater toxicity than the pure compound in adults.
Conclusions:
- Parathion disrupts spermatogenesis by increasing germ cell apoptosis.
- The pesticide likely interferes with DNA, RNA, and protein synthesis.
- The observed effects of parathion-induced apoptosis are reversible with moderate doses after acute exposure.