naphthoquinones and 2-methyl-4-chlorophenoxy-gamma-butyric-acid

Pesticide exposure during fetal life can lead to low birth weight and is commonly observed in reproductive toxicology studies. Associations have also been found in low birth weight babies born from pesticide-exposed gardeners. Since low birth weight is also linked to metabolic disorders, it can be speculated that early life exposure to pesticides could increase the risk of becoming obese or developing diabetes later in life. We have analyzed potential long-term effects of gestational and lactational exposure to a low dose mixture of six pesticides that individually can cause low birth weight: Cyromazine, MCPB, Pirimicarb, Quinoclamine, Thiram, and Ziram. Exposed male offspring, who were smaller than controls, displayed some degree of catch-up growth. Insulin and glucagon regulation was not significantly affected, and analyses of liver and pancreas did not reveal obvious histopathological effects. Efforts towards identifying potential biomarkers of metabolic disease-risk did not result in any strong candidates, albeit leptin levels were altered in exposed animals. In fat tissues, the key genes Lep, Nmb and Nmbr were altered in high dosed offspring, and were differentially expressed between sexes. Our results suggest that early-life exposure to pesticides may contribute to the development of metabolic disorders later in life.

Topics: 2-Methyl-4-chlorophenoxyacetic Acid; Adipose Tissue; Animals; Butyrates; Carbamates; Diabetes Mellitus; Female; Fetal Growth Retardation; Infant, Low Birth Weight; Naphthoquinones; Pesticides; Pregnancy; Prenatal Exposure Delayed Effects; Pyrimidines; Rats; Rats, Wistar; Thiram; Triazines; Ziram