Chronic exposure to low doses of bisphenol A alters hydromineral responses in rats

Bisphenol A (BPA) is a chemical commonly used in the industrial sectors, hence humans are exposed to the compound repetitively. BPA is an endocrine disruptor and has been anticipated to interfere on chemical estrogen receptor functions and other nuclear hormone receptors. Estrogens are steroid hormones that, in addition to their neuroendocrine roles, affect water and salt intakes in numerous species, including humans and rodents. Changes in the hydrosaline balance produce compensatory behavioral and physiological responses, which serve to preserve or restore osmolarity and blood volume to optimal levels, thus preventing cardiovascular disease. The aim of the present work was to determine for first time the effect of long-term and low-dose BPA treatment on thirst and sodium appetite. Wistar rats were exposed to BPA via drinking water to mimic the most likely route of human exposure, and different dipsogenic and natriorexigenic stimuli were assessed. The BPA-treated rats tend to drink less water that control rats following 24-h fluid restriction, but there was no statistically significant decrease. Perhaps the BPA dose does not have enough estrogenic potency to affect water intake. In the extracellular fluid depletion test, the control rats significantly increased 2.7% NaCl solution intake on repeated testing, showing sodium appetite sensitization, i.e. the capacity to enhance sodium intake produced by stimulus repetition; whereas BPA-treated rats did not. In this study, fluid and electrolyte balance in BPA-treated rats is generally adequate but impaired in osmotic challenges, for example by sodium depletion. Thus, neuroendocrine systems involved in maintaining body fluid and electrolyte homeostasis were altered in BPA-treated rats.