Adnan Berk Dinçsoy

Background: Doxorubicin (dox) is a chemotherapeutic agent widely used against various tumors. However, the clinical use of this agent is limited due to various organ toxicities. Taurine is an intracellular free β-amino acid with antioxidant properties. The present study investigated the protective mechanism of taurine on dox-induced hepatotoxicity. Methods: In total, 31 male Sprague-Dawley rats were used in the study. The control group received intraperitoneal (i.p.) 0.9% NaCl alone for 14 days; the taurine (Tau) group received i.p. taurine 150 mg/kg body weight/day for 14 days; the dox group received dox on days 12, 13, and 14 at a cumulative dose of 25 mg/kg body weight/3 days; and the tau+dox group received taurine and dox together at the same dose and through the same route. On day 15, biochemical evaluations were performed on blood samples taken from the left ventricle followed by histological examinations on liver samples. Results: Dox was found to increase liver function enzymes and tissue protein carbonyl levels, causing congestion and tissue damage, thereby leading to dysfunction. Tau was found to histologically preserve the liver morphology without showing any corrective effect on oxidative stress parameters. These findings suggest that the membrane-stabilizing effect of taurine may be more effective than its radical scavenging activity in preventing dox-induced toxicity. Conclusion: Taurine can prevent doxorubicin-induced hepatotoxicity through non-antioxidant pathways.

To the Editor, In previous issues of the journal, we have just read with great interest the paper by chen entitled “Empagliflozin attenuates doxorubicin- induced cardiotoxicity by activating AMPK/SIRT-1/PGC-1α- mediated mitochondrial biogenesis” published in Toxicology Research; 2023, 1–8. ¹ The study showed us that doxorubicin induced cardiomyopathy can be ameliorated by a empagliflozin by activating AMPK/SIRT-1/PGC-1α- mediated mitochondrial biogenesis clearly. And, in this letter, we would like to convey our contribution to this paper. First of all, congratulations to the author for this beautiful work. Because in our previous study, it was shown by electron microscopy that doxorubicin impaired mitochondrial biogenesis and empagliflozin restored it. ² We had suggested that the pathophysiologic pathway of this condition might be due to the increase in PGC1 α levels by empagliflozin, but we could not prove it. In this study, the researcher has completed the missing part of our study by showing that PGC1 α levels increase with empagliflozin. We thank him for this contribution.