Why the study?
Studies suggest oxidative stress-induced toxic changes due to DOX administration, prompting evaluation of the protective effect of N-acetylcysteine against DOX oxidative damage.
Does N-acetylcysteine prevent doxorubicin-induced oxidative stress in heart tissue of rats?
Does N-acetylcysteine prevent doxorubicin-induced oxidative stress in heart tissue of rats?
N-acetylcysteine demonstrates cardioprotective effects against doxorubicin-induced cardiotoxicity in a rat model by modulating oxidative stress and the antioxidant redox system.
NAC may protect against DOX-induced rat liver oxidative stress; leaves open clinical translation in cancer patients.
Doxorubicin (DOX) is a chemotherapeutic agent and is widely used in cancer treatment. There are some studies suggesting oxidative stress-induced toxic changes in the liver due to DOX administration. The aim of this study was to reveal the oxidative damage of DOX in liver tissue at molecular level and to evaluate the protective effect of N-acetylcysteine (NAC) against DOX oxidative damage. Twenty four rats weighing 150-200 g were randomly divided into four equal groups; group I : control, group 2: received a single dose of DOX, group 3: received NAC for 28 days and group 4: received a single dose of DOX, followed by NAC for 28 days. At the end of the experiment, heart tissues were taken from all animals. Malondialdehyde (MDA), Total Antioxidant Capacity (TAC), Total Oxidant Capacity (TOC) levels were determined in these samples by spectrophotometric methods. It was determined that TOC level increased, TAC levels decreased in the group given DOX compared to the control group. In addition, TAC levels increased in the DOX+NAC group (p0.05). It was concluded that DOX administration increased oxidative stress and NAC administration could prevent it. NAC caused modulatory effects on oxidative stress and antioxidant redox system in DOX-induced heart toxicity in the rat.
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Çakına et al. (2024) studied this question.
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