24 research outputs found
Reactive oxygen species and male reproductive hormones
Reports of the increasing incidence of male infertility paired with decreasing semen quality have triggered studies
on the effects of lifestyle and environmental factors on the male reproductive potential. There are numerous exogenous
and endogenous factors that are able to induce excessive production of reactive oxygen species (ROS) beyond that of
cellular antioxidant capacity, thus causing oxidative stress. In turn, oxidative stress negatively affects male reproductive
functions and may induce infertility either directly or indirectly by affecting the hypothalamus-pituitary-gonadal (HPG)
axis and/or disrupting its crosstalk with other hormonal axes. This review discusses the important exogenous and
endogenous factors leading to the generation of ROS in different parts of the male reproductive tract. It also highlights
the negative impact of oxidative stress on the regulation and cross-talk between the reproductive hormones. It further
describes the mechanism of ROS-induced derangement of male reproductive hormonal profiles that could ultimately
lead to male infertility. An understanding of the disruptive effects of ROS on male reproductive hormones would
encourage further investigations directed towards the prevention of ROS-mediated hormonal imbalances, which in turn
could help in the management of male infertility
Healing of osteoporotic vertebral compression fractures following cure of Cushing's syndrome
Identification of a novel mutation of the PRKAR1A gene in a patient with Carney complex with significant osteoporosis and recurrent fractures
Proposals for prevention and management of steroid-induced osteoporosis in children and adolescents
Competitive light-initiated chemiluminescent assay: using 5-α-dihydrotestosterone-BSA as competitive antigen for quantitation of total testosterone in human sera
Changes in glucocorticoid receptor immunoreactivity after adrenalectomy and corticosterone treatment in the rat testis
Modulation in Wistar rats of blood corticosterone compartmentation by sex and prior exposure to a cafeteria diet
In the metabolic syndrome, glucocorticoid activity is increased, but circulating levels show little change. Most of blood glucocorticoids are bound to corticosteroid-binding globulin (CBG), which liver expression and circulating levels are higher in females than in males. Since blood hormones are also bound to blood cells, and the size of this compartment is considerable for androgens and estrogens, we analyzed whether sex or eating a cafeteria diet altered the compartmentation of corticosterone in rat blood. The main corticosterone compartment in rat blood is that specifically bound to plasma proteins, with smaller compartments bound to blood cells or free. Cafeteria diet increased the expression of liver CBG gene, binding plasma capacity and the proportion of blood cell-bound corticosterone. There were marked sex differences in blood corticosterone compartmentation in rats, which were unrelated to testosterone. The use of a monoclonal antibody ELISA and a polyclonal Western blot for plasma CBG compared with both specific plasma binding of corticosterone and CBG gene expression suggested the existence of different forms of CBG, with varying affinities for corticosterone in males and females, since ELISA data showed higher plasma CBG for males, but binding and Western blot analyses (plus liver gene expression) and higher physiological effectiveness for females. Good cross- reactivity to the antigen for polyclonal CBG antibody suggests that in all cases we were measuring CBG.The different immunoreactivity and binding affinity may help explain the marked sex-related differences in plasma hormone binding as sex-linked different proportions of CBG forms