Some environmental contaminants interact with hormones and may exert adverse consequences due to their actions as endocrine disrupting chemicals (EDCs). Exposure in people is typically due to contamination of the food chain, inhalation of contaminated house dust, or occupational exposure. EDCs include pesticides and herbicides (such as diphenyl-dichloro-trichloroethane, DDT, or its metabolites), methoxychlor, biocides, heat stabilizers and chemical catalysts (such as tributyltin, TBT), plastic contaminants (e.g. bisphenol A, BPA), pharmaceuticals (i.e. diethylstilbestrol, DES; 17alpha-ethynilestradiol, EE2), or dietary components (such as phytoestrogens). The goal of this review is to address sources, effects and actions of EDCs, with an emphasis on topics discussed at the International Congress on Steroids and the Nervous System. EDCs may alter reproductively-relevant or non-reproductive, sexually-dimorphic behaviors. In addition, EDCs may have significant effects on neurodevelopmental processes, influencing morphology of sexually-dimorphic cerebral circuits. Exposure to EDCs is more dangerous if it occurs during specific “critical periods” of life, such as intrauterine, perinatal, juvenile or puberty periods, when organisms are more sensitive to hormonal disruption, than in other periods. However, exposure to EDCs in adulthood also can alter physiology. Several EDCs are xenoestrogens, may alter serum lipid concentrations, or metabolism enzymes that are necessary for converting cholesterol to steroid hormones, ultimately altering production of E2 and/or other steroids. Finally, many EDCs may have actions via, or independent of, classic actions at cognate steroid receptors. EDCs may have effects through numerous other substrates, such as the aryl hydrocarbon receptor (AhR), the peroxisome proliferator-activated receptor (PPAR) and retinoid X receptor (RXR), signal transduction pathways, calcium influx, and/or neurotransmitter receptors. Thus, EDCs, from varied sources, may have organizational effects during development, and/or activational effects in adulthood, that influence sexually-dimorphic, reproductively-relevant processes or other functions, by mimicking, antagonizing, or altering steroidal actions.

Perinatal action of estrogens or aromatizable steroids at the central nervous system level is responsible for brain sexual differentiation. Through early contact with the central nervous system, the estrogenic compound bisphenol A (BPA) could alter the processes affecting sociosexual behavior. To test this hypothesis, we studied agonistic and sexual behavior of adult female and male rats whose mothers were administered BPA (40 microg/kg/day) during pregnancy or lactation. An intruder test revealed in males but not in females an increase in defensive behavior due to BPA. We studied the effect of BPA on sexual behavior by testing sexual orientation and sexual activity. Male sexual orientation toward a stimulus female was not affected by BPA, whereas the sexual activity test revealed a slight impairment of sexual performance due to BPA in terms of latency and frequency of intromissions. In females, BPA produced a small increase in sexual motivation and receptive behavior. In conclusion, BPA administration, both during pregnancy and during lactation, does not masculinize female behavior or potentiate masculinization processes of males. On the contrary, we observed a potentiation of female behavior in females and a depotentiation of male behavior in males.

Bisphenol A (BPA) is an environmental estrogen with potentially averse effects on public health. We studied the long-term effects of perinatal exposure to BPA on later behavior in adult rats of both sexes. BPA or vehicle was administered orally to mother rats from mating to pups' weaning, at a concentration (0.040 mg/kg) within the range of human exposure. The offspring of both sexes were tested at adolescence (postnatal days 35-45) for novelty preference (experiment 1). After a 3-day familiarization to one side of a two-chamber apparatus, on day 4 rats were allowed to freely explore the whole apparatus. BPA-exposed females spent significantly less time than did controls in exploration of the novel side (i.e., increased neophobia), whereas no effect was found in the male group. At adulthood, the same animals were food deprived and tested for profiles of impulsive behavior (experiment 2), in operant chambers provided with two nose-poking holes (delivering either five or one food pellet). After the establishment of a baseline preference for the large reinforcer, a delay was introduced before the delivery of the five food pellets, which was progressively increased each day (10, 20, 30, 45, 60, 80, 100 sec). As expected, all animals exhibited a progressive shift toward the immediate but smaller reinforcer. A reduced level of impulsive behavior (i.e., a shift to the right in the intolerance-delay curve) was evidenced in BPA-treated rats. The frequency of inadequate responding (during the length of the delay) also provided a measure of restless behavior. Interestingly, the profile of BPA-treated males was feminized, strongly resembling that of control females. Animals were then tested (experiment 3) for the response to an amphetamine challenge (1 mg/kg, subcutaneously). The drug-induced increment activity was significantly less marked in BPA-treated male rats compared with controls. These findings provide clear indirect evidence of long-term alterations in brain monoaminergic function after perinatal BPA exposure. This may be a cause for concern for public health, confirming that exposure to a weak environmental estrogen in the period of sexual differentiation of the brain can influence adult behavior.

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Insight regarding the genetic origin and composition of the studied population of the red-legged partridge (Alectoris rufa) is likely to provide general and critical information for the appropriate management and possible conservation of the species. The reintroduced population of red-legged partridges living in Pianosa Island (National Park Tuscany Archipelago) has proven to be sustainable: captive-bred individuals, morphologically assigned to the taxon A. rufa, were released to the island approximately 20 years ago, establishing an apparently well-adapted population. We have investigated this population by means of 10 microsatellite loci in order to shed light on its genetic structure. Considering that A. rufa is known to crossbreed with A. chukar, the Pianosa Island population was compared at the molecular level with a red-legged partridge breeding stock (Aulla, MS) as well as with a population of pure A. chukar. Our results indicate that the red-legged partridge population from Pianosa, morphologically identified as A. rufa, is actually partly introgressed with A. chukar, questioning its genetic purity and the possible use of this population as a starting stock for future reintroductions elsewhere.

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