Key result
Diosmin plus CoQ10 cuts doxorubicin-induced ALT elevation ~24% in preclinical hepatorenal toxicity.
Why the study?
Doxorubicin perturbs mitochondrial structure and function in tumor and cardiac cells, causing therapeutic effects and toxic side effects, but more understanding of mitochondrial impact is needed.
Effect estimate: 24% decline
Absolute Event Rate: 103.4% vs 136.5%
p-value: p=<0.05
Should not change doxorubicin use in patients; leaves open need for human trials on hepatorenal protection.
BACKGROUND: The mitochondria may very well determine the final commitment of the cell to death, particularly in times of energy stress. Cancer chemotherapeutics such as the anthracycline doxorubicin perturb mitochondrial structure and function in tumour cells, as evidenced in osteosarcoma, for which doxorubicin is used clinically as frontline therapy. This same mechanism of cell inhibition is also pertinent to doxorubicin's primary cause of side-effects, that to the cardiac tissue, culminating in such dire events as congestive heart failure. Reactive oxygen species are partly to blame for this effect on the mitochondria, which impact the electron transport chain. OBJECTIVE: As this review highlights that, there is much more to be learnt about the mitochondria and how it is affected by such effective but toxic drugs as doxorubicin. CONCLUSION: Such information will aid researchers who search for cancer treatment able to preserve mitochondrial number and function in normal cells.
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Crispin R. Dass (2018) studied Doxorubicin-induced hepatorenal toxicity (n=40). Diosmin and Coenzyme Q10 vs. Doxorubicin alone (2.5 mg/kg i.p. every other day) was evaluated on Serum Alanine Aminotransferase (ALT) levels (U/dl) (24% decline, p=<0.05).
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