Stress factors such as hyperthermia, microorganism infection and exposure to heavy metals inhibit spermatogenesis, but the mechanisms involved remain poorly understood. In February 15 Journal of Clinical Investigation, Nobuaki Ozawa and colleagues from Keio University, Tokyo, Japan show that heme oxygenase-1 (HO-1) derived from Leydig cells in the testis regulates apoptosis of premeiotic spermatocytes in response to stress.

Ozawa et al. exposed rats to cadmium chloride (CdCl2) — a stressor causing oligozoospermia — and monitored the induction of HO-1, a carbon monoxide-generating enzyme. They found that CdCl2-elicited HO-1 occurred mostly in Leydig cells, generated CO and induced apoptosis in the diploid and tetraploid germ cells from the peripheral regions of seminiferous tubules. In addition, inhibition of HO with zinc protoporphyrin-IX prevented these effects, while supplementation with a CO donor restored the apoptosis (J Clin Invest 2002, 109:457-467).

These data raises the...

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