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Doxorubicin: the good, the bad and the ugly effect.
TLDR
The mechanisms underlying not only DOX beneficial effects but also its toxic outcomes are discussed, and some potential strategies to attenuate DOX-induced toxicity will be debated. Expand
Doxorubicin‐Induced Cardiotoxicity: From Bioenergetic Failure and Cell Death to Cardiomyopathy
TLDR
What is known about some of the potential mechanisms of DOX‐induced cardiotoxicity including mitochondrial oxidative damage and loss of cardiomyocytes are discussed and pharmaceutical and nonpharmaceutical approaches that may decrease DOX cardiac alterations in animal models and humans are presented. Expand
Diabetes and the impairment of reproductive function: possible role of mitochondria and reactive oxygen species.
TLDR
The impact of Diabetes and associated oxidative stress on sexual function is highlighted, and maternal diabetes during pregnancy is associated with an increased risk of complications in the offspring, such as altered fetal growth, polyhydramnios, fetal loss and congenital malformations. Expand
Moderate endurance training prevents doxorubicin-induced in vivo mitochondriopathy and reduces the development of cardiac apoptosis.
TLDR
It is concluded that endurance training protects heart mitochondrial respiratory function from the toxic effects of DOX, probably by improving mitochondrial and cell defense systems and reducing cell oxidative stress. Expand
Drug-induced cardiac mitochondrial toxicity and protection: from doxorubicin to carvedilol.
TLDR
The two referred examples result in important take-home messages: drug-induced cardiac mitochondrial dysfunction is an important contributor for drug-associated organ failure, protection of mitochondrial function is involved in the beneficial impact of some clinically-used drugs and a more accurate prediction of toxic vs. beneficial effects should be an important component of drug development by the pharmaceutical industry. Expand
Role of mitochondria in nonalcoholic fatty liver disease--from origin to propagation.
TLDR
The role of mitochondrial dysfunction in critical initiating or propagating events in fatty liver infiltration and nonalcoholic fatty liver disease (NAFLD) is examined and mitochondrial metabolic remodeling is a predominant factor in the appearance and perpetuation of hepatocyte fat accumulation. Expand
Investigating drug-induced mitochondrial toxicity: a biosensor to increase drug safety?
TLDR
The assessment of "mitochondrial safety" for new discovered molecules is of clear interest for pharmaceutical companies which can now select compounds lacking mitochondrial toxicity to undergo further trials, thus avoiding the possibility of later human toxicity due to mitochondrial liabilities. Expand
Acute exercise protects against calcium-induced cardiac mitochondrial permeability transition pore opening in doxorubicin-treated rats.
TLDR
It is demonstrated that acute exercise protects against cardiac mitochondrial dysfunction, preserving mitochondrial phosphorylation capacity and attenuating DOX-induced decreased tolerance to MPTP opening. Expand
Enhanced permeability transition explains the reduced calcium uptake in cardiac mitochondria from streptozotocin‐induced diabetic rats
TLDR
The results show that streptozotocin diabetes facilitates the mitochondrial permeability transition in cardiac mitochondria, resulting in decreased mitochondrial calcium accumulation, and that heart mitochondria from diabetic rats had depressed oxygen consumption during the phosphorylative state. Expand
Physical exercise prior and during treatment reduces sub-chronic doxorubicin-induced mitochondrial toxicity and oxidative stress.
TLDR
Both chronic models of physical exercise performed before and during the course of sub-chronic DOX treatment translated into an improved mitochondrial bioenergetic fitness, which may result in part from the prevention of mitochondrial oxidative stress and damage. Expand
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