Co-consumption of selenium and vitamin E altered the reproductive and developmental toxicity of methylmercury in rats.
Methylmercury (MeHg), an environmental contaminant primarily found in fish and seafood, may pose long-term health risks to pregnant women and their developing children. The objective of this study was to determine whether co-consumption of nutritional supplements would alter the effects of MeHg on reproductive and developmental toxicity using a rodent model. Adult female rats were fed a diet containing additional selenium (1 ppm), additional vitamin E (225 IU/kg) or a combination of the two for 4 weeks before oral dosing of MeHg (1.25 mg/kg/day). Treatment with MeHg and dietary supplementation continued throughout pregnancy after which the dams were allowed to deliver their offspring. In addition to routine evaluations including periodic body weight measurements and daily clinical signs observations, dams and pups were evaluated for auditory startle habituation and pups were evaluated for developmental landmarks and reflexology. The dams and offspring were euthanized approximately 4 weeks after birth of the offspring. Results indicated that treatment with MeHg caused adverse effects on both reproduction of the dams and decreased progeny survival. However, the dams showed significant improvement in body weight gain during lactation and average auditory startle response time when the diet was enriched with both selenium and vitamin E. The combination of both vitamin E and Se also resulted in a significant increase in post-natal survival when compared to MeHg-treated group. There was no nutrient effect on the MeHg toxicity shown in offspring physical landmarks, performance in reflex tests and assessment of simple auricular startle response. Also, accelerated development as indicated by earlier opening in the pups of the supplemental diet groups was observed. These results suggest that antioxidant nutrients in the diet may alter MeHg reproductive and developmental toxicity. The underlying and human health implications warrant further investigations.
Beyrouty
Peter
P
Department of Natural Resource Sciences, McGill University, Ste.-Anne-de-Bellevue, Montreal, Quebec, Canada.
Chan
Hing Man
HM
D000284:Administration, Oral; D000818:Animals; D000831:Animals, Newborn; D001835:Body Weight / Q000187:drug effects; D001921:Brain / Q000187:drug effects / Q000254:growth & development / Q000503:physiopathology; D004195:Disease Models, Animal; D004338:Drug Combinations; D004347:Drug Interactions; D005260:Female; D008297:Male; D020262:Mercury Poisoning, Nervous System / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D008767:Methylmercury Compounds / Q000037:antagonists & inhibitors* / Q000633:toxicity; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D051381:Rats; D017207:Rats, Sprague-Dawley; D013216:Reflex, Startle / Q000187:drug effects; D012098:Reproduction / Q000187:drug effects; D012643:Selenium / Q000494:pharmacology* / Q000627:therapeutic use; D015996:Survival Rate; D016896:Treatment Outcome; D014810:Vitamin E / Q000494:pharmacology* / Q000627:therapeutic use
D004338:Drug Combinations; D008767:Methylmercury Compounds; D014810:Vitamin E; D012643:Selenium