N-Acetylcysteine prevents doxorubucine-induced cardiotoxicity in rats

Abstract

This study is designed to observe the effects of N-acetylcysteine (NAC) on doxorubucine-induced cardiac toxicity in rats both histologically and biochemically. Totally 32 rats divided equally into four groups were studied. The first group received only 200 mg/kg NAC intraperitoneal (i.p.) once every 24 h for 5 days (group 1); the second group received 20 mg/kg doxorubucine (DOX) i.p. single dose plus NAC 200 mg/kg i.p. once every 24 h for 5 days (group 2); the third group received DOX 20 mg/kg DOX i.p. single dose (group 3) and the fourth group, which is also the control group, received saline (group 4). Following 24 h of the final dose, blood samples were drawn from a portal vein and heart tissue were obtained. Tissue thiobarbituric acid reactive substance (TBARS) and nitric oxide (NO) levels were highest in the DOX group. In the DOX-treated rats, serum TBARS, NO, aspartate transaminase, lactate dehydrogenase and creatine kinase levels were highest when compared with other groups. Except for serum superoxide dismutase levels, all other parameters differed significantly between the DOX plus NAC group and the DOX group. In the DOX plus NAC group, general architecture was preserved better than the DOX group and myofibril loss was minimal compared with the DOX group. NAC demonstrated, both biochemically and histologically, to be effective in the prevention of DOX-induced cardiotoxicity in rat models. Evaluation of NAC's effect on DOX toxicity warrants further clinical trials on cancer patients.

Study of the Cardiotoxicity of Venenum Bufonis in Rats using an 1H NMR-Based Metabolomics Approach

“…Significantly increased levels of serum CK, γ-GT, FFA, MDA and ROS were found in groups given VB compared with the NC group. As a reliable indicator of myocardial injury, the serum CK level peaked at 6 hr after the administration of VB, consistent with previous reports [ 27 , 28 ]. The liver toxicity of VB was demonstrated by the presence of significantly elevated γ-GT levels, complemented by pathological evaluation of the liver.…”

Protective effect of N-acetylcysteine on cyclophosphamide-induced cardiotoxicity in rats

“…NAC has a strong cardioprotective effect, decreases lipid peroxidation in the heart tissue and prevents free radicals-induced damage to the myocardium by its free radical scavenging effect (Arica et al, 2013;Nagoor Meeran and Mainzen Prince, 2011). On the other hand, Gurbuz et al (2009) reported that, NAC protects against CPinduced genotoxic damage due to their antioxidant, nucleophilic properties and to the ability to act as precursors of glutathione.…”

“…Group II: rats were treated with NAC (200 mg/kg, i.p.) for 5 consecutive days (Arica et al, 2013). Group III: rats were injected i.p.…”

“…NAC acts as a precursor for GSH biosynthesis as well as a stimulator of the cytosolic enzymes involved in glutathione regeneration (Shivalingappa et al, 2012). NAC has a protective effect against isoproterenol-induced cardiotoxicity (Nagoor Meeran and Mainzen Prince, 2011) and doxorubicin-induced cardiac damage (Arica et al, 2013). NAC have been found to have diverse therapeutic actions including vasodilation effect due to an increase in cyclic guanosine monophosphate levels, platelet aggregation inhibition, sulphydryl group donation to regenerate endothelial-derived relaxing factor and reduces in IL-8 and TNF-␣ production (Kekec et al, 2010).…”

Beneficial effects of carnosine and carnosine plus vitamin E treatments on doxorubicin-induced oxidative stress and cardiac, hepatic, and renal toxicity in rats

“…Our results reported here agree with those of previous studies, which showed that DOX produces a prooxidant status in the tissues of rats. [2][3][4][5][6][7][8][9][10][11][12] CAR and related derivatives of histidine are found in high concentrations in cardiac muscle. CAR is considered a multifunctional molecule with antioxidant action and operates as a selective inhibitor of protein glycation and protein-protein cross-linking.…”