Related Experiment Videos
In utero and lactational exposure of carbofuran to rats: effect on testes and sperm
N Pant1, R Shankar, S P Srivastava
1Industrial Toxicology Research Centre, Lucknow, India.
Abstract:
Male offspring of adult females treated with 0.2 or 0.4 mg/kg during either the whole of pregnancy or the whole of the lactation period did not induce generalised toxic effects. A significant alteration in enzymatic activities i.e. SDH (decreased), LDH and Y-GT (increased) were observed in testes only at 0.4 mg/kg. A decrease in sperm motility, sperm count along with increase in percent abnormal sperm was observed at 0.4 mg/kg dose level. Histopathological examination revealed loss of spermato-genesis, degenerative changes in Sertoli cells which are well supported with biochemical studies indicating that carbofuran interferes with the maturation process of testis. No such effects were observed at 0.2 mg/kg. The testicular and spermatotoxic effects observed in rats given in utero or lactational exposure may be due to transfer of carbofuran or its metabolites through placenta or mothers milk.
Insights
Prenatal or lactational exposure to carbofuran at 0.4 mg/kg caused significant testicular toxicity in male offspring, including reduced sperm quality and altered enzyme activity. No adverse effects were seen at 0.2 mg/kg.
Area of Science:
- Toxicology
- Reproductive Toxicology
- Environmental Health
Background:
- Pesticide exposure during critical developmental windows can impact reproductive health.
- Carbofuran is a widely used pesticide with known toxicological properties.
Purpose of the Study:
- To investigate the potential testicular and spermatotoxic effects of carbofuran exposure in male offspring following in utero or lactational exposure.
- To determine dose-dependent effects and identify a no-observed-adverse-effect level (NOAEL) for carbofuran's reproductive toxicity.
Main Methods:
- Pregnant and lactating rats were administered carbofuran at 0.2 or 0.4 mg/kg.
- Offspring testes were analyzed for enzymatic activities (SDH, LDH, Y-GT).
- Sperm parameters (motility, count, abnormalities) and testicular histopathology were evaluated.
Main Results:
- Carbofuran at 0.4 mg/kg significantly decreased sperm motility and count, increased abnormal sperm, and altered testicular enzyme activities (decreased SDH, increased LDH, Y-GT).
- Histopathology revealed impaired spermatogenesis and Sertoli cell degeneration at 0.4 mg/kg.
- No significant toxicological or spermatotoxic effects were observed at the 0.2 mg/kg dose.
Conclusions:
- Carbofuran exposure during pregnancy or lactation at 0.4 mg/kg induces significant testicular toxicity and impairs sperm maturation in male offspring.
- These effects are likely mediated by the transfer of carbofuran or its metabolites via the placenta or maternal milk.
- The 0.2 mg/kg dose appears to be a safe level regarding these specific reproductive endpoints.