Dehydroepiandrosterone (DHEA) possesses fat-reducing effect, while little information is available on whether DHEA regulates cell proliferation and mitochondrial function, which would, in turn, affect lipid droplet accumulation in the broiler. In the present study, the lipid droplet accumulation, cell proliferation, cell cycle and mitochondrial membrane potential were analysis in primary chicken hepatocytes after DHEA treated. The results showed that total area and counts of lipid droplets were significantly decreased in hepatocytes treated with DHEA. The cell viability was significantly increased, while cell proliferation was significantly inhibited in a dose-dependent manner in primary chicken hepatocytes after DHEA treated. DHEA treatment significantly increased the cell population in S phase and decreased the population in G2/M in primary chicken hepatocytes. Meanwhile, the cyclin A and cyclin-dependent kinases 2 (CDK2) mRNA abundance were significantly decreased in hepatocytes after DHEA treated. No significant differences were observed in the number of mitochondria, while the mitochondrial membrane permeability and succinate dehydrogenase (SDH) activity were significantly increased in hepatocytes after DHEA treated. In conclusion, our results demonstrated that DHEA reduced lipid droplet accumulation by inhibiting hepatocytes proliferation and enhancing mitochondrial function in primary chicken hepatocytes.

Hydrogen sulfide (H 2 S) could availably regulate electron transport in the inner membrane of mitochondria from bovine heart when succinate as substrate and rotenone as complex I inhibitor at 37°C were used. H 2 S increased to a certain extent the respiratory rate of state 4. It also increased first and then decreased the respiratory rate of state 3, respiratory control ratio and ADP/O ratio. In addition, it quicken first and then delayed recovery time from state 3 to state 4. The effects of H 2 S as aforementioned in normoxic condition were more obvious than those in hypoxic condition. Experimental results indicated that more than 10 μM H 2 S brought about uncoupling of mitochondrial electron transport and the opening of mitochondrial K ATP channel located in complex III-IV, and less than 10 μM H 2 S unexpectedly facilitated this course, which might be via sulfide-quinone oxidoreductase. The finding that H 2 S was closely related with sulfide-quinone oxidoreductase, however, requires in depth investigation.