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This work analyzed possible dopamine-mediated cadmium effects on plasma prolactin, GH and ACTH levels and if these changes were related to metal accumulation. Male rats were treated from day 30 to 60 of life with 50 mg/L of CdCl2 in the drinking water. Cadmium exposure decreased the dopamine (DA) metabolism (DOPAC/DA ratio) in all brain areas studied, and plasma levels of prolactin, GH and ACTH were diminished. The cadmium concentration did not increase nor in hypothalamus nor in the pituitary after the metal exposure. These results suggest that cadmium inhibits the secretion of these pituitary hormones and this inhibitory effect is not mediated by dopamine or the degree of metal accumulation.

This paper analyzes possible dopamine (DA) mediated cadmium effects on plasma levels of prolactin, growing hormone (GH) and adrenocorticotropic hormone (ACTH), and if these changes are related to metal accumulation. For that purpose, adult male rats were treated with 50 mg/L of CdCl2 in the drinking water for one month. Plasma levels of prolactin, ACTH and GH were measured by specific double antibody radioimmunoassays. DA was measured by high performance liquid chromatography using electrochemical detection. Cadmium content in the tissues was measured by atomic absorption spectometry with graphite furnace. Analysis was performed by using a T-Student test. Metal exposure increased DA content (34.79+/-3.06 vs. 18.2+/-2.88 pg/mg protein) and decreased its turnover (0.40+/-0.07 vs. 0.75+/-0.06) in posterior hypothalamus. Cadmium also decreased DA turnover in median eminence (0.48+/-0.15 vs. 1.50+/-0.63). Plasma levels of prolactin and GH decreased (2.4+/-0.11 vs. 3.1+/-0.15 ng/mL and 5.37+/-0.05 vs. 9.87+/-1.8 ng/mL respectively), while those of ACTH increased (2.73+/-0.14 vs. 1.7+/-0.16 ng/mL). Cadmium concentration increased in both hypothalamus (4.88+/-0.34 vs. 0.72+/-0.2 microg/g) and pituitary (22.82+/-4.57 vs. 5.02+/-1.25 microg/g) after the metal exposure. These results suggest that cadmium effects on the secretion of these hormones are not mediated by dopamine and might be correlated to the metal accumulation at pituitary level.

Methoxychlor (MTX) is a pesticide currently used as a substitute for dichloro-diphenyl-trichloroethane (DDT). This organochloride insecticide has some estrogenic properties, and may modify the feedback mechanisms of steroids on the hypothalamus and pituitary. This work was undertaken to explore the possible effects of MTX on the episodic prolactin release and to analyze whether these effects are mediated by dopamine (DA), luteinizing hormone (LH), and/or testosterone. Adult male Sprague-Dawley rats were administered 25 mg/kg/day of MTX in sesame oil for 30 days. Control animals received vehicle only. The episodic prolactin release and plasma testosterone levels were measured as well as the dopamine (DA) content in the median eminence (ME) and in the anterior (AH), mediobasal (MBH), and posterior (PH) hypothalamus. The mean serum prolactin levels and absolute pulse amplitude of the hormone increased after the xenobiotic administration, whereas its relative pulse amplitude diminished. The frequency and duration of prolactin peaks and its half-life were not modified by the treatment with the pesticide. On the other hand, methoxychlor decreased the DA content in ME, increased it in AH, and did not change it in MBH or PH. MTX decreased plasma levels of LH and testosterone compared with controls. These data suggest estrogenic and antiandrogenic effects of MTX on the episodic prolactin secretion; the changes observed in prolactin release could be explained, at least in part, by some of the changes of DA at the hypothalamus and of LH at the pituitary, but not by changes of testosterone at the testicular level.

This study was undertaken to analyze if the effects of subchronic alternating cadmium exposure on pituitary hormone secretion are mediated by changes in dopamine turnover in an age dependent way or are directly correlated to cadmium accumulation at the hypothalamic-pituitary axis. Male rats were treated sc. from day 30 to 60 (prepubertal period) or from day 60 to 90 (adult age) of life, with cadmium chloride (CdCl2) at a dose of 0.5 and 1.0 mg kg(-1) bw, every 4th day in an alternate schedule, starting with the smaller dose. Dopamine (DA) turnover, expressed as the ratio of acid 3.3-dihidroxifenil acetic (DOPAC)/DA in various hypothalamic areas, the plasma levels of prolactin, growth hormone (GH) and adrenocorticotropic hormone (ACTH), and cadmium accumulation in the hypothalamus and pituitary were studied. Prepubertal cadmium exposure decreased DA content in all hypothalamic areas studied, although its turnover was not modified. A decrease in plasma ACTH levels with no changes in plasma prolactin and GH levels were found. Cadmium did not accumulate in pituitary while it increased in the hypothalamus. Metal exposure during adulthood decreased DA content in mediobasal and posterior hypothalamus, and its turnover in posterior hypothalamus and median eminence. It decreased plasma prolactin and ACTH levels but not those of GH. Cadmium concentration increased in both hypothalamus and pituitary. These results suggest that cadmium exposure produces age dependent changes on the secretory mechanisms of the pituitary hormones studied, related to the selective accumulation of the metal at both hypothalamic and hypophyseal level changes. However the effects of the metal are not mediated by dopamine.

Cadmium increases or decreases prolactin secretion depending on the dose and duration of the exposure to the metal. However, whether there are cadmium effects on the episodic prolactin secretion is less well known. This study was undertaken to address whether chronic alternating exposure to two different doses of cadmium affects the episodic pattern of prolactin and to what extent the effects of cadmium are age-dependent. Male rats were treated s.c. with cadmium chloride (0.5 or 1.0 mg/kg) from day 30 to 60, or from day 60 to 90 of age, with alteration of the doses every 4 days, starting with the smaller dose. Controls received vehicle every 4 days. The last dose of cadmium was given 48 h prior to the pulsatility study. Prolactin secretion in the 4 experimental groups studied was episodic and changed significantly after cadmium exposure. Cadmium administration from day 30 to 60 of life significantly decreased the mean half-life of prolactin. On the other hand, when administered from day 60 to 90 cadmium significantly decreased the mean as well as serum prolactin levels and the absolute amplitude of the prolactin pulses, their duration, the relative amplitude or the mean half-life of the hormone. The frequency of prolactin peaks was not changed by cadmium administration. The results indicate that low intermittent doses of cadmium chronically administered change the episodic secretion pattern of prolactin in rats. The effects of cadmium on prolactin secretion were age dependent.

This work was undertaken to assess if exposure to cadmium related to puberty may affect the episodic pattern of prolactin. Male rats were submitted to cadmium exposure, from day 30 to 60 or from day 60 to 90 of life respectively, at a dose of 50 ppm in the drinking water. Control age-matched rats received cadmium-free water. Prepubertal cadmium administration decreased mean serum prolactin levels and the absolute amplitude of the prolactin pulses. Subchronic exposure to cadmium of adult rats decreased mean serum prolactin levels, the absolute amplitude of the prolactin pulses and their duration, and the mean half-life of the hormone. These results suggest that subchronic cadmium exposure changes the secretory pattern of prolactin in adult male rats in a puberty-dependent way.