In utero and neonate exposure to nonylphenol develops hyperadrenalism and metabolic syndrome later in life. I. First generation rats (F(1))

Abstract

Nonylphenol (NP) is an endocrine disruptor (ENDR). It is a chemical associated with the production and degradation of nonylphenol ethoxylates (NPE). NPE is widely used as nonionic surfactants. Previously, we observed that NP increased the production of corticosterone and aldosterone from zona fasciculata-reticularis, and zona glomerulosa cells, respectively. By the "fetal origins adult diseases" (Barker hypothesis), we examined the possible impact of NP exposure during developmental (in utero and neonatal) period with focus on disturbed adrenal function and related hyperadrenal syndrome, i.e. Cushings syndrome/metabolic syndrome. In this study, female rats drink NP water during pregnancy and lactation conferred F(1) generation: (1) increase the corticosterone, aldosterone concentration in plasma; (2) increase 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activity in liver and adipose tissue; (3) increase aldosterone synthase activity in adrenal for adult offspring. Furthermore, it can increase body weight, adrenocorticotropin (ACTH) concentration in plasma, 11β-HSD1 protein expression in liver, steroidogenic acute regulatory (StAR) protein expression and 11β-hydroxylase activity in adrenal for male adult offspring. In summary, NP exposure during developmental period bestowed F(1) generation with hyperadrenalism and its consequence of metabolic syndrome.