Perinatal exposure to phthalates and susceptibility to prostatic inflammation in adulthood

• Grant number: 24/06915-5
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: October 01, 2024
• End date: September 30, 2026
• Field of knowledge: Health Sciences - Medicine - Pathological Anatomy and Clinical Pathology
• Principal Investigator: Cristiane Figueiredo Pinho
• Grantee: Maria Clara Betete da Silva Fonseca
• Host Institution: Faculdade de Ciências (FC). Universidade Estadual Paulista (UNESP). Campus de Bauru. Bauru , SP, Brazil

Abstract

Phthalates are synthetic esters widely used as additives in the manufacturing of plastic products, being present in the composition of food packaging, clothes, paints, and personal care items. These compounds were classified as emerging environmental pollutants, which can cause several morphological, metabolic and reproductive alterations in exposed organisms, especially in hormone-dependent organs such as the prostate. Recent research has correlated phthalates with the establishment of prostatic inflammatory processes, which could contribute to the development of diseases such as prostatitis and prostate cancer. In this context, the present study aims to evaluate the late effects of perinatal exposure to an environmentally relevant mixture of phthalates on the prostate structure, as well as tissue molecular markers involved in the inflammation process. For this, pregnant Sprague-Dawley rats will be treated with a mixture of six different phthalates [DEHP (Bis(2-ethylhexyl) phthalate), DEP (Diethyl phthalate), DBP (Di-n-butyl phthalate), DiBP (Diisobutyl phthalate), BBP (Butylbenzyl phthalate) and DiNP (Diisononyl phthalate)] from gestational day 12 to postnatal day 21, by daily gavage, at doses of 0µg, 20µg, 200µg and 200mg/kg. On postnatal day 120, the offspring will be euthanized and the dorsolateral prostate of each male will be removed, weighed and processed histologically for histopathological analysis of the lesions, quantification of mast cells, and immunostaining for NFºB, TNF-± and TLR4 (inflammatory mediators).