Clinically, impaired reproductive development has been demonstrated in the sons of female gardeners or farmers who have been exposed to pesticides. Humans and wild animals are exposed to MXC mostly MNI-caged-D-aspartate through the dietary intake of contaminated food. Higher concentrations of MXC have been found in human milk, elevating the demand for assessing the risk of offspring after maternal exposure to MXC. To clarify the molecular mechanisms of exposure to MXC on male reproduction, we conducted a study examining MXC exposure during the perinatal period to determine its effect on fetal development, as well as the long-term impacts on the male reproductive systems of C57BL/6 mice. Although, it is widely accepted that EDCs have a great influence on human and animal reproduction at toxicological doses, the knowledge on the exposure of humans to lower or environmentally relevant doses of EDCs or of related effects on offspring remains limited. The present study was carried out to investigate the mechanisms responsible for the adverse effects of low-dose MXC exposure during the perinatal period, allowing for a better understanding of the mechanisms behind these histological abnormalities in the prepubertal period. Our results demonstrated that perinatal exposure to low-dose MXC could impair the testes development, not only by disturbing testicular Leydig cell proliferation but also by interrupting steroidogenesis and spermatogenesis. Previous experiments have demonstrated that exposure to organochlorine pesticides might induce intrauterine growth retardation and obesity in puberty. Prenatal exposure to low doses of MXC reduces the postnatal growth. Consistently, we found that the exposure to low doses of MXC perinatally decreased body weight at P0.5 and MIRA-1 increased body weight at P45.5, thus we assumed obesity as one of the putative reasons for the differential body weights among the groups on P45.5. As IUGR has been linked to increased metabolic syndrome risk later in life, the study of low doses of MXC exposure leading to metabolic syndrome needs to be further investigated. Many experiments have demonstrated that estrogen or estrogenic substances can conversely inhibit steroidogenic genes, such as Star, Cyp11a1 and Cyp17a1. HPTE, a metabolite of MXC, possesses ERa agonist activity. In the present study, we found that Cyp11a1 and T levels were decreased, but Cyp19a1 and E2 levels were increased. Therefore, MXC could regulate Cyp19a1 expression, and in turn leads to an increase in E2 production. However, how the MXC disturbs the expression of steroidogenic genes is still unknown. The balance of androgenic and estrogenic signals plays a key role in the male reproductive system. Our lab previous results demonstrated that the mice overexpressing human aromatase possessed a multiple structural and functional alterations in the reproductive organs.