Abstract
Cadmium (Cd) is regarded as a potential endocrine disruptor. However, the exact mechanism by which this metal may interfere with the reproductive system has not yet been elucidated. The present study aimed to investigate the effect of subacute Cd oral administration at daily doses of 0.09, 1.8, and 4.5 mgCd/kg b.w. and the impact of Cd on sex hormones (estradiol (E2) and progesterone (P)) in the plasma and uterus, as well as on estrous cyclicity and histopathological changes in uterine and ovary in female rats after terminating the exposure and after a prolonged observation period (3 months). Moreover, Cd bioaccumulation in the uterine and brain tissue of rats was analyzed. The study revealed that oral Cd exposure induced changes in the plasma levels of steroid hormones: decrease in E2 and increase in P after the highest dose of Cd. Probably, for the first time, it was evidenced that circulation sex hormone disturbances in Cd-exposed rats caused irregular estrous cycle, persisting for 3 months after exposure termination; no alterations in these hormone levels in uterine tissue were noted. Cd did not induce estradiol-like hyperplasia of endometrium, but resulted in endometrial edema irrespective of the dose, and caused damage of the ovaries after the highest dose. In summary, subacute oral exposure of female rats to Cd may lead to long-term disturbances in reproductive system.
Highlights
Cadmium (Cd) is a toxic metal characterized by extensive persistence in the environment
In the positive control group, the uterine weight did not statistically increase after 30 days of 17βestradiol administration, the tendency to increase the weight persisted for 3 months after the end of exposure in comparison to oil control (Table 2)
The results show that Cd after 30 days of oral administration affects circulating sex hormones, and what is significant, the changes we observed persisted even up to 3 months after terminating the exposure, especially after the highest administered dose
Summary
Cadmium (Cd) is a toxic metal characterized by extensive persistence in the environment. Exposure to Cd occurs mainly via food, water, and tobacco smoking (WHO 1992; EFSA 2012). Environ Sci Pollut Res (2018) 25:28025–28038 environmental endocrine disruptors (EDs), which are defined as Bexogenous substances or mixtures, that alter function(s) of endocrine system and cause adverse health effects in an intact organism, or its progeny, or (sub)populations^ (WHO/IPCS 2002). Later studies confirmed that Cd chronic exposure does disturb the reproductive endocrine function but may lead to the reduction in testicular mass, generative alterations in testes (Nolan and Shaikh 1986; Toman and Massányi 2002; Ciarrocca et al 2013; de Angelis et al 2017), and decreased spermatozoa mobility (Lukáč et al 2003)
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