Effects of Dibromochioropropane Upon Diurnal Variations of Gonadotropins and Androgens

Cortés-Gallegos, V.; G, Castañeda; Alonso, R; Arellano, Hortensia; Cervantes, C. Escobar; Parra, Adalberto

doi:10.1002/j.1939-4640.1980.tb00042.x

Cited by 14 publications

(6 citation statements)

References 4 publications

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“…The reduced plasma androgens and E2 concentrations found after the restless period could represent an adaptative response to the acute stress and certainly is not due to a methodology artifact, since the hormonal concentrations observed in the phase 1 (control) closely agree with those previously reported from our laboratory [2,4] as well as with those reported by others [lo, 161. The lack of significant changes in C levels could be explained in several ways: a) It is an emergency reaction to maintain corticosteroid synthesis as normal as possible; b) An acute sleep deprivation present only once may not be sufficient to induce any detectable changes and; c) The peripheral cortisol concentrations are not necessarily linked to the sleep phenomenon [ 191.…”

Section: Discussionsupporting

confidence: 89%

Sleep Deprivation Reduces Circulating Androgens in Healthy Men

Cortés-Gallegos

Alonso

et al. 1983

Archives of Andrology

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The acute effect of sleep deprivation on the pituitary-testis axis was evaluated in 13 healthy men. To study such association, the circulating levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin (PRL), Androstenedione (A), Testosterone (T), Dihydrotestosterone (DHT) and Estradiol (E2) were measured along with Cortisol (C) before and after sleep deprivation. Morning (8:OO AM) venous blood samples were obtained prior and after a continuous restless period of 24 hr and the values were analyzed by the paired Student's r test. There was a significant and parallel decrease of each androgen and E2 but not of FSH, LH.PRL, or C, associated with the acute sleep deprivation.

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Section: Discussionsupporting

confidence: 89%

Sleep Deprivation Reduces Circulating Androgens in Healthy Men

Cortés-Gallegos

Alonso

et al. 1983

Archives of Andrology

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“…It obviously is not due to a methodology artifact, since the hormonal concentrations observed in phase I (control) closely agree with those previously reported from our laboratory [3] as well with those reported by others [7, 91. However, this hormonal change could be secondary to an increased metabolic clearance rate, a shortened circulating half-life, a decrease of the sex hormone binding protein, or a true reduction on testicular steroidogenesis. This information needs to be ascertained among other factors by combining the role of catecholamines from the sympatho-adrenal neuroendocrine system [6].…”

Section: Discussionsupporting

confidence: 92%

Disturbing the Light-Darkness Pattern Reduces Circulating Testosterone in Healthy Men

Cortés-Gallegos

Aranda

Pelaez

1998

Archives of Andrology

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“…LC hyperplasia has been reported in men exposed to DBCP and confirmed histologically (Cortes-Gallegos et al, 1980). In men showing classic symptoms of male reproductive toxicity from DBCP exposure, investigators reported increased LH levels with normal testosterone levels.…”

Section: Dibromochloropropane (Dbcp)mentioning

confidence: 86%

“…In contrast to nongenotoxic agents, the only genotoxic agents that have any hormonal or mechanistic data are cadmium (Bomhard et al, 1987;Laskey and Phelps, 1991;Waalkes and Rehm, 1992), dibromochloropropane (DBCP) (Cortes-Gallegos et al, 1980;), and radiation (Lindsay et al, 1969;Pinon-Lataillade et al, 1991). These compounds are discussed below.…”

Section: B Genotoxic Compoundsmentioning

confidence: 95%

“…For instance, DBCP has been shown to produce LC hyperplasia in humans, presumably secondary to tubule damage. In rodents, DBCP only produces testicular atrophy (Cortes-Gallegos et al, 1980) and, consistent with DBCP being a genotoxic agent, induces multiple tumors at sites other than the testis in oncogenicity studies with mice and rats (Whorton and Foliart, 1983). The isoprene and methyl-CCNU studies were 1 year and 70 days in duration, respectively; hence, their inability to induce tumors at other sites is in all likelihood a reflection of the short study duration (Melnick et al, 1994;Yegana et al, 1988).…”

Section: Radiationmentioning

confidence: 99%

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Rodent Leydig Cell Tumorigenesis: A Review of the Physiology, Pathology, Mechanisms, and Relevance to Humans

Cook

Klinefelter

Hardisty

et al. 1999

Critical Reviews in Toxicology

175

122

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Leydig cells (LCs) are the cells of the testis that have as their primary function the production of testosterone. LCs are a common target of compounds tested in rodent carcinogenicity bioassays. The number of reviews on Leydig cell tumors (LCTs) has increased in recent years because of its common occurrence in rodent bioassays and the importance in assessing the relevance of this tumor type to humans. To date, there have been no comprehensive reviews to identify all the compounds that have been shown to induce LCTs in rodents or has any review systematically evaluated the epidemiology data to determine whether humans were at increased risk for developing LCTs from exposure to these agents. This review attempts to fill these deficiencies in the literature by comparing the cytology and ontogeny of the LC, as well as the endocrine and paracrine regulation of both normal and tumorigenic LCs. In addition, the pathology of LCTs in rodents and humans is compared, compounds that induce LC hyperplasia or tumors are enumerated, and the human relevance of chemical-induced LCTs is discussed. There are plausible mechanisms for the chemical induction of LCTs, as typified by agonists of estrogen, gonadotropin releasing hormone (GnRH), and dopamine receptors, androgen receptor antagonists, and inhibitors of 5alpha-reductase, testosterone biosynthesis, and aromatase. Most of these ultimately involve elevation in serum luteinizing hormone (LH) and/or LC responsiveness to LH as proximate mediators. It is expected that further work will uncover additional mechanisms by which LCTs may arise, especially the role of growth factors in modulating LC tumorigenesis. Regarding human relevance, the pathways for regulation of the hypothalamo-pituitary-testis (HPT) axis of rats and humans are similar, such that compounds that either decrease testosterone or estradiol levels or their recognition will increase LH levels. Hence, compounds that induce LCTs in rats by disruption of the HPT axis pose a risk to human health, except for possibly two classes of compounds (GnRH and dopamine agonists). Because GnRH and prolactin receptors are either not expressed or are expressed at very low levels in the testes in humans, the induction of LCTs in rats by GnRH and dopamine agonists would appear not to be relevant to humans; however, the potential relevance to humans of the remaining five pathways of LCT induction cannot be ruled out. Therefore, the central issue becomes what is the relative sensitivity between rat and human LCs in their response to increased LH levels; specifically, is the proliferative stimulus initiated by increased levels of LH attenuated, similar, or enhanced in human vs. rat LCs? There are several lines of evidence that suggest that human LCs are quantitatively less sensitive than rats in their proliferative response to LH, and hence in their sensitivity to chemically induced LCTs. This evidence includes the following: (1) the human incidence of LCTs is much lower than in rodents even when corrected for detection bias; (2) several ...

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Effects of Dibromochioropropane Upon Diurnal Variations of Gonadotropins and Androgens

Cited by 14 publications

References 4 publications

Sleep Deprivation Reduces Circulating Androgens in Healthy Men

Sleep Deprivation Reduces Circulating Androgens in Healthy Men

Disturbing the Light-Darkness Pattern Reduces Circulating Testosterone in Healthy Men

Rodent Leydig Cell Tumorigenesis: A Review of the Physiology, Pathology, Mechanisms, and Relevance to Humans

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