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Steroid Hormone Metabolism (steroid + hormone_metabolism)

Distribution by Scientific Domains

Medical Sciences	50%

Selected Abstracts

An evolutionary concept for altered steroid hormone metabolism in patients with rheumatoid arthritis

EXPERIMENTAL DERMATOLOGY, Issue 2 2005
Rainer H. Straub
The pathogenesis of chronic disabling inflammatory diseases (CDIDs) is partly understood. The presently used concepts focus mainly on abnormalities of the immune system but this view is incomplete. The presented concept is a new framework for the pathogenesis of CDIDs. It integrates evolutionary theories with the classical immunological standpoint, which is further linked with a neuroendocrine immune view of erroneous homeostatic adaptation of the other supersystems (nervous system, endocrine system, reproductive system): 1. In CDIDs, the loss of tolerance against self and harmless foreign antigens leads to continuous immune aggression which is dependent on a multifactorial genetically polymorph background (the initiation). 2. However, advantageous or disadvantageous adaptation to CDIDs were not evolutionary conserved because CDIDs severely impaired reproduction or appeared after the reproductive phase and, thus, imply a strong negative selection pressure. 3. Reactions of all supersystems are evolutionary conserved for transient inflammatory reactions such as the elimination of infectious agents, wound healing, foreign body reaction and many others. 4. The sum of the false reactions of all supersystems , conserved for transient inflammation , provide the pathogenetic background for the chronification of CDIDs because a continuous aggressive situation is created (the chronification). The human disease of rheumatoid arthritis is used as a prototypic CDID to illustrate the integrated view point. The synovial tissue innervation is in the focus of this concept. [source]

Effect of lindane on CYP-mediated steroid hormone metabolism in male mice following in utero exposure

JOURNAL OF APPLIED TOXICOLOGY, Issue 8 2009
Emma Di Consiglio
Abstract A wide number of pesticides, including highly persistent organochlorinated compounds, such as lindane (LIN), may induce reproductive and developmental alterations by directly binding to the estrogen/androgen receptors or altering steroid hormone metabolism. In the present work, we have investigated whether LIN in utero exposure of CD1 mice affects the reproductive system in male offspring by causing an impairment of the CYP-dependent steroid hormone metabolism. Dam exposure to 25 mg kg,1 b.w. LIN occurred during critical developmental periods, from gestational days 9 to 16. Effects on hepatic CYP-mediated testosterone (TST) hydroxylase, aromatase activities and testicular parameters were tested at postnatal days (PND 50, 65,69, 100) that are critical for sexual maturation in CD1 mice. In the adult F1 mice significant changes of male reproductive endpoints (testis weight, spermatid number) as well as dramatic effects on CYP-mediated TST metabolism were observed on PND 65,69, in the absence of any of systemic toxicity. The levels of TST 6, - and 2, -hydroxylation and dehydrogenation showed the highest level of reduction, suggesting CYP 3A and 2C families as the major target of LIN induced effects. All changes were almost recovered on PND 100. No effects on aromatase activity were evidenced. Overall, these findings provide useful information for a better characterization of the LIN mode of action. They suggest that LIN-induced toxicity in males is linked to an impairment of steroid hormone homeostasis, due to CYP-mediated TST catabolism modulation and differs from LIN receptor-mediated mechanism previously reported in females. Copyright © 2009 John Wiley & Sons, Ltd. [source]

Obesity and polycystic ovary syndrome

CLINICAL ENDOCRINOLOGY, Issue 2 2006
T. M. Barber
Summary The aetiology of Polycystic Ovary Syndrome (PCOS) is complex and multifactorial. There is much evidence, however, to suggest that adipose tissue plays an important role in the development and maintenance of PCOS pathology. There is a close correlation between adiposity and symptom severity in women with PCOS, and even modest reductions in weight generally translate into significant improvements in menstrual regularity, fertility and hyperandrogenic features. This review article considers the various mechanisms that might underlie this link between excess adiposity and PCOS , including the effects of differential insulin sensitivity, abnormal steroid hormone metabolism and adipocytokine secretion. Greater attention to the therapeutic options available to reduce the impact of excess adiposity on ovarian and metabolic function is essential to the management of PCOS. [source]