Endocrine Abstracts

Mitochondria play a key role in hormone biosynthesis and involve in renal cell proliferation by producing about 90% of cellular energy and controlling cell apoptosis. Doxorubicin is commonly used for many tumor treatments. However, its clinical utility is limited by the adverse reactions, which are known to be nephrotoxic. The mechanism by which doxorubicin induced kidney damage is still not completely understood, however nephrotoxicity by doxorubicin might be related to mitochondrial dysfunction. In this experiment, the following mitochondrial toxicity test was performed after doxorubicin was treated to mouse kidney stem cells. First, we identified IC₅₀ values for doxorubicin in mouse kidney cells. We investigated that mRNA expression level of Mn-SOD, the neutralizer of reactive oxygen species (ROS), in the mitochondria increased in a concentration-dependent manner of doxorubicin. To confirm the relationship between mitochondrial toxicity and ROS, MitoSOX red assay was performed. The results showed that the ROS level increased according to the ascending concentration of doxorubicin. Further experiment should be conducted for assessing the apoptosis pathway induced by doxorubicin. This research was supported by grants (20183MFDS525) from the Ministry of Food and Drug Safety in 2021.