Developmental toxicity caused by environmental exposure to heavy metals during the perinatal period has raised questions about offspring health. Cadmium (Cd) is an endocrine-disrupting chemical with the potential to interfere with morphogenesis and susceptibility to diseases in reproductive organs. Taking into account that in the rat prostate morphogenesis occurs during the perinatal period, and that pregnant females absorb and retain more dietary Cd than their non-pregnant counterparts, it is important to understand the effects of perinatal Cd exposure on the adult rat prostate. Therefore this study investigated the effects of gestational and lactational Cd exposure on adult offspring rat prostate histopathology. Pregnant rats (n = 20) were divided into two groups: Control (treated with aqueous solution of sodium acetate 10 mg/l) and treated (treated with aqueous solution of cadmium acetate 10 mg/l) administered in the drinking water. After weaning, male offspring from different litters (n = 10) received food and water 'ad libitum'. The animals were euthanized at postnatal day 90 (PND90), the ventral prostates (VPs) were removed, weighed and examined histopathologically. Blood was collected for the measurement of testosterone (T) levels. Immunohistochemistry for androgen receptor (AR) and Ki67, and a TUNEL assay were performed. There were no differences in T levels, cell proliferation and apoptosis indexes, or AR immunostaining between the experimental groups. Stromal inflammatory foci and multifocal inflammation increased significantly in the treated group. These changes were associated with inflammatory reactive epithelial atypia and stromal fibrillar rearrangement. In conclusion, VP was permanently affected by perinatal Cd exposition, with increased incidence of inflammatory disorders with ageing.
Silver nanoparticles
(AgNPs) have potent antimicrobial activity
and, for this reason, are incorporated into a variety of products,
raising concern about their potential risks and impacts on human health
and the environment. The developmental period is highly dependent
on thyroid hormones (THs), and puberty is a sensitive period, where
changes in the hormonal environment may have permanent effects. We
evaluated the hypothalamic–pituitary (HP)–thyroid axis
after exposure to low doses of AgNPs using a validated protocol to
assess pubertal development and thyroid function in immature male
rats. For stimulatory events of the HP–thyroid axis, we observed
an increase in the expression of Trh mRNA and serum
triiodothyronine. Negative feedback reduced the hypothalamic expression
of Dio2 mRNA and increased the expression of Thra1, Thra2, and Thrb2 mRNAs. In the pituitary,
there was a reduced expression of Mct-8 mRNA and Dio2 mRNA. For peripheral T3-target tissues, a reduced expression
of Mct-8 mRNA was observed in the heart and liver.
An increased expression of Dio3 mRNA was observed
in the heart and liver, and an increased expression of Thrb2 mRNA was observed in the liver. The quantitative proteomic profile
of the thyroid gland indicated a reduction in cytoskeletal proteins
(Cap1, Cav1, Lasp1, Marcks, and Tpm4; 1.875 μg AgNP/kg) and
a reduction in the profile of chaperones (Hsp90aa1, Hsp90ab1, Hspa8,
Hspa9, P4hb) and proteins that participate in the N-glycosylation
process (Ddost, Rpn1 and Rpn2) (15 μg AgNP/kg). Exposure to
low doses of AgNPs during the window of puberty development affects
the regulation of the HP–thyroid axis with further consequences
in thyroid gland physiology.
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