The effects of N-acetylcysteine on cisplatin induced cardiotoxicity

Abstract

OBJECTIVES: Recent studies reported that oxidative stress is an important mechanism that contributes to cisplatin induced cardiotoxicity. In the present study, the effects of N-acetylcysteine (NAC), which is an antioxidant, on cisplatin induced cardiotoxicity were investigated in a rat model. METHODS: Thirty two rats were separated into 4 equal groups: Control, NAC-250, CP (cisplatin), CP+NAC. Rats in the experimental groups were treated with a single dose of cisplatin intraperitoneally (ip) (10 mg/kg) and NAC (ip, 250 mg/kg) for 3 consecutive days. At the end of the experiment, cardiotoxicity was determined from plasma CK-MB, LDH, cTnI and cardiac myosin light chain-1 (CMLC-1) levels. In the tissue samples, total oxidant capacity (TOC), total antioxidant capacity (TAC), lipid hydroperoxide (ROOH) and thiol levels were measured. The hearts were also analyzed histopathologically. RESULTS: It was determined that cisplatin increased the tissue TOC, ROOH levels and decreased TAC and thiol levels. NAC administration after cisplatin treatment was observed to have ameliorated histological and functional changes in heart. CONCLUSIONS: In conclusion, the results of this experimental study suggested that oxidative stress had a serious effect on cisplatin cardiotoxicity, and NAC could be used as a therapeutic agent in addition to standard cisplatin treatment protocols (Tab.

Antioxidant effect of acetyl-l-carnitine against cisplatin-induced cardiotoxicity

“…CDDP increases the total oxidant capacity in tissues. 31,32 One weakness of our study was that we could not perform electrocardiography or echocardiography in mice because of the unavailability of equipment. Another disadvantage might be that we did not use an ALCAR monotherapy group.…”

Hesperidin protects against cisplatin-induced cardiotoxicity in mice by regulating the p62–Keap1–Nrf2 pathway

“…CP has serious cardiotoxicity and other side effects. [27][28][29] As a result, many tumour patients have to stop taking CP early, and the desired therapeutic effect is not achieved. Therefore, new therapeutic agents with better cardiac protection and safety to attenuate CP-induced cardiotoxicity are required.…”

Cardioprotective effect of all-trans retinoic acid on cisplatin induced cardiotoxicity in rats

“…There are some other therapeutic agents which have documented cardioprotective effects on cisplatin induced cardiotoxicity such as N-acetyl cysteine, taurine, coenzyme Q, trimetazidine and rutin 13-17-18-25 . Gunturk et al 25 investigated the effects of Nacetylcysteine (NAC), which is an antioxidant, on cisplatin induced cardiotoxicity in a rat model and they showed that in the CP+NAC group, interstitial edemaand vacuolization was at a significantly lower level than seen in the cisplatin group and hemorrhage was improved in the CP+NAC group compared to the cisplatin only group, but was still high. While in the present study, edema was also more severe in the CP group than the ATRA + CP group but there was a statistically significant difference in the severity of hemorrhage between the ATRA group and the CP and the ATRA + CP groups.…”