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Paternal effects from methamidophos administration in mice
V R Burruel1, O G Raabe, J W Overstreet
1Institute of Toxicology and Environmental Health, University of California, Davis 95616, USA.
Abstract:
In this study, the mouse was used to evaluate paternal germline exposure to the organophosphate methamidophos for its potential to produce adverse effects on spermatozoa and in the offspring. There have been reports that organophosphate exposure can increase abnormal sperm morphology in mice. However, effects transmitted to the offspring following paternal exposure have not been reported previously. The maximum tolerated dose (MTD) was 7.5 mg kg(-1) body weight and this dose resulted in no deaths, although blood plasma cholinesterase activity was still decreased. Males were euthanized 4 weeks after an acute intraperitoneal injection of methamidophos (0.5, 3.75, 5.0, and 7.5 mg kg(-1) body wt) and the number of spermatids per gram testes and sperm morphology were analyzed. In this study, abnormal sperm morphology on a per group basis exhibited a dose-response significantly related to increased methamidophos exposure as indicated by regression analysis and a nested ANOVA (p < 0.0001). Preimplantation embryos that were conceived 6 weeks after paternal methamidophos exposure (5 mg kg(-1) body wt) exhibited a significant increase in cleavage arrest. Fertility of males was also affected as shown by a decrease in the number of two- to four-cell embryos per male (postexposure week 6) and an increase in the number of degenerated embryos (postexposure weeks 4-6). We conclude that methamidophos may have the potential to produce transmissible adverse embryonic effects following an acute paternal germline exposure.
Insights
Paternal exposure to the organophosphate methamidophos can cause abnormal sperm and harm offspring development. This study found methamidophos exposure in male mice led to adverse effects on sperm and early embryonic development.
Area of Science:
- Environmental Toxicology
- Reproductive Toxicology
- Developmental Toxicology
Background:
- Organophosphate exposure is linked to increased abnormal sperm morphology in mice.
- Effects of paternal organophosphate exposure on offspring have not been previously reported.
Purpose of the Study:
- To evaluate the potential adverse effects of paternal germline exposure to methamidophos on spermatozoa and offspring.
- To investigate transmissible embryonic effects following acute paternal germline exposure.
Main Methods:
- Male mice were exposed to varying doses of methamidophos (0.5-7.5 mg/kg).
- Spermatid count, sperm morphology, and embryonic development (cleavage arrest, degeneration) were analyzed post-exposure.
- Statistical analyses included regression and nested ANOVA to determine dose-response relationships.
Main Results:
- Abnormal sperm morphology showed a significant dose-response relationship with increased methamidophos exposure (p < 0.0001).
- Preimplantation embryos from exposed males exhibited increased cleavage arrest and degeneration.
- Male fertility was affected, with decreased two- to four-cell embryos and increased degenerated embryos.
Conclusions:
- Methamidophos exposure can induce abnormal sperm morphology.
- Acute paternal germline exposure to methamidophos may lead to transmissible adverse embryonic effects.
- Further research is warranted to understand the long-term implications of such exposures.
