Prepubertal male rats with high rates of germ-cell apoptosis present exacerbated rates of germ-cell apoptosis after serotonin depletion

• DOI: 10.1071/rd13382
• Publication Date: 2014-11-20T00:52:24Z
• Authors: Néstor Méndez Pal...; María Elena Ayala...; Maximino Méndez M...; Rubén Huerta Crispín; Octavio Guerrero ...; Javier Hernández ...; Andrés Aragón Mar...
• Keywords: Male; 0301 basic medicine; Serotonin; Progesterone Reductase; Gene Expression Regulation, Developmental; Apoptosis; Receptors, Cell Surface; Hydroxyindoleacetic Acid; Spermatogonia; Rats; Kinetics; Random Allocation; 03 medical and health sciences; Serotonin Agents; Proto-Oncogene Proteins c-bcl-2; Receptors, Androgen; Animals; RNA, Messenger; Sexual Maturation; Spermatogenesis; p-Chloroamphetamine; bcl-2-Associated X Protein

Male germ-cell apoptosis occurs naturally and can be increased by exposure to drugs and toxic chemicals. Individuals may have different rates of apoptosis and are likely to also exhibit differential sensitivity to outside influences. Previously, we reported that p-chloroamphetamine (pCA), a substance that inhibits serotonin synthesis, induced germ-cell apoptosis in prepubertal male rats. Here, we identified prepubertal rats with naturally high or low rates of germ-cell apoptosis and evaluated gene expression in both groups. Bax and Shbg mRNA levels were higher in rats with high rates of germ-cell apoptosis. Rats were then treated with pCA and the neuro-hormonal response and gene expression were evaluated. Treatment with pCA induced a reduction in serotonin concentrations but levels of sex hormones and gonadotrophins were not changed. Rats with initially high rates of germ-cell apoptosis had even higher rates of germ-cell apoptosis after treatment with pCA. In rats with high rates of germ-cell apoptosis Bax mRNA expression remained high after treatment with pCA. On the basis of category, an inverse relationship between mRNA expression of Bax and Bcl2, Bax and AR and Bax and Hsd3b2 was found. Here we provide evidence that innate levels of germ-cell apoptosis could be explained by the level of mRNA expression of genes involved with apoptosis and spermatogenesis.