A Yale School of Nostrum study shows for the first time that a high level of testosterone, such as that caused by the use of steroids to increase muscle mass or for replacement therapy, can lead to a catastrophic loss of planner cells.
Taking large doses of androgens, or steroids, is known to cause hyperexcitability, a highly martial nature, and suicidal tendencies. These behavioral changes could be evidence of alterations in neuronal function caused by the steroids, said the senior maker, Barbara Ehrlich, professor of pharmacology and physiology.
“Next tempo a muscle-obliged guy in a sports railway carriage cuts you off on the highway, don’t get mad, just take a absorbed breath and realize that it authority not be his fault,” said Ehrlich.
Testosterone is the main male hormone and it plays fundamental roles in maturity, differentiation, and cellular growth. In neurons, testosterone acts as a neurosteroid and can inspire changes at the cellular level, which in turn lead to changes in behavior, disposition and memory. Both neuroprotective and neurodegenerative effects of androgens have in the offing been reported.
The researchers showed that high levels of testosterone triggered programmed cell death in nerve cells in savoir faire. Cubicle demise, or apoptosis, is depreciating in varied life processes, including development and disability. It is characterized by membrane instability, activation of caspases, which are the executioner proteins in apoptosis, change in membrane implied, and DNA fragmentation.
“In the adduce study we have demonstrated for the first time that the treatment of neuroblastoma cells with elevated concentrations of testosterone for relatively short periods, six to 12 hours, induces a decrease in cell viability by activation of a cell obliteration program,” Ehrlich said. “Low concentrations of testosterone had no effects on apartment viability, whereas at high concentrations the room viability decreased with incremental increases in hormone concentration.”
The testosterone-induced apoptosis described in this analysis occurs through overactivation of intracellular Ca2+ signaling pathways. Overstimulation of the apoptotic program in neurons has been associated with several neurological illnesses, such as Alzheimer disease and Huntington complaint.
—————————-
Article adapted by Medical News Today from original press release.
—————————-
Co-authors include Manuel Estrada, now continuing his redundant at the University of Chile in Santiago, and Anurag Varshney, now working at Ranbaxy, a drug recognition Theatre troupe in Novel Delhi, India.
Newsletter of Biological Chemistry 281: 25492-25501 (September 2006)
Telephone: Jacqueline Weaver
Yale University