Mitochondrial transplantation attenuates toxicity in rat renal proximal tubular cells caused by Favipiravir.

OBJECTIVES

Exogenous mitochondria transplantation or mitotherapy can be used to swap out unhealthy mitochondria for functioning ones. Treatment of mitochondrial diseases using this approach may be beneficial.

METHODS

In this study, we looked at the effect of transplanting newly isolated mitochondria on the toxicity that favipiravir (FAV) causes in renal proximal tubular cells (RPTCs). In this study, parameters such as lactate dehydrogenase (LDH) leakiness, reactive oxygen species (ROSs) production, damage to the lysosome membrane, reduced glutathione (GSH) content, extracellular oxidized glutathione (GSSG) content, GSH/GSSG ratio, ATP level, mitochondrial membrane potential (MMP) collapse, Bcl-2 content, and caspase-3 activity were used to assess the protective effects of mitochondrial transplantation against FAV-induced mitochondrial toxicity.

KEY FINDINGS

The statistical analysis showed that the cytotoxicity, ROS production, MMP collapse, lysosomal damage, GSSG levels, and caspase-3 activity brought on by FAV in RPTCs were reduced by transplanting the healthy mitochondria. In addition, it led to an increase in ATP level, GSH content, Bcl-2 content, and GSH/GSSG ratio in RPTCs.

CONCLUSIONS

A recent study found that mitochondrial transplantation is a powerful therapeutic approach for treating nephrotoxicity brought on by xenobiotics.