Mitochondrion Participated in Effect Mechanism of Manganese Poisoning on Heat Shock Protein and Ultrastructure of Testes in Chickens.

Abstract

Manganese (Mn) poisoning can happen in the case of environmental pollution and occupational exposure. However, the underlying mechanisms of Mn-induced teste toxicity and whether mitochondrion and heat shock proteins (HSPs) are involved in toxic effect of Mn on chicken testes remain poorly understood. To investigate this, MnCl2·4H2O was administered in the diet (600, 900, and 1800mg/kg Mn) of chickens for 30, 60, and 90days. Electron microscopy and qPCR were performed. Results showed that Mn exposure suppressed dose- and time-dependently HSP40 and HSP60 mRNA levels, meanwhile increased does-dependently HSP27, HSP70, and HSP90 mRNA levels at all three time points under three Mn exposure concentrations. Furthermore, Mn treatment damaged myoid cells, spermatocytes, and Sertoli cells through electron microscopic observation, indicating that Mn treatment damaged chicken testes. In addition, abnormal shapes of mitochondria were found, and mitochondria displayed extensive vacuolation. The increase of HSP90 and HSP70 induced by Mn exposure inhibited HSP40 and stimulated HSP27, respectively, in chicken testes, which needs further to be explored. Taken together, our study suggested that there was toxic effect in excess Mn on chickens, and HSPs and mitochondria were involved in the mechanism of dose-dependent injury caused by Mn in chicken testes. This study provided new insights for Mn toxicity identification in animal husbandry production practice.