N-acetylcysteine versus progesterone on the cisplatin-induced peripheral neurotoxicity

Zaki, Sherif Mohamed; Mohamed, Eman A.; Motawie, A G; Fattah, Shereen Abdel

doi:10.5603/fm.a2017.0090

Cited by 21 publications

(17 citation statements)

References 54 publications

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“…In the study of Zaki and coworkers [38] it is obvious that peripheral neurotoxicity was induced following prolonged cisplatin administration with a cumulative dose that was twice as high as the dose applied in this study (16 mg/kg vs. 7.5 mg/kg). A similar observation could be made for NAC supplementation.…”

Section: Discussionmentioning

confidence: 72%

N-Acetylcysteine Protects against the Anxiogenic Response to Cisplatin in Rats

et al. 2019

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Since cisplatin therapy is usually accompanied with numerous toxicities, including neurotoxicity, that involve tissue oxidative damage, the aim of this study was to evaluate the possible protective effect of N-acetylcysteine (NAC) on the anxiogenic response to cisplatin (CIS). Thirty-two male Wistar albino rats divided into four groups (control, cisplatin, NAC, and CIS + NAC). All treatments were delivered intraperitoneally. On day one, the control and cisplatin groups received saline while the NAC and CIS + NAC groups were administered with NAC (500 mg/kg). On the fifth day, the control group received saline while the CIS group was treated with cisplatin (7.5 mg/kg), the NAC group again received NAC (500 mg/kg), and the CIS + NAC group was simultaneously treated with cisplatin and NAC (7.5 and 500 mg/kg, respectively). Behavioral testing, performed on the tenth day in the open field (OF) and elevated plus maze (EPM) tests, revealed the anxiogenic effect of cisplatin that was significantly attenuated by NAC. The hippocampal sections evaluation showed increased oxidative stress (increased lipid peroxidation and decline in antioxidant enzymes activity) and proapoptotic action (predominantly by diminished antiapoptotic gene expression) following a single dose of cisplatin. NAC supplementation along with cisplatin administration reversed the prooxidative and proapoptotic effects of cisplatin. In conclusion, the results obtained in this study confirmed that antioxidant supplementation with NAC may attenuate the cisplatin-induced anxiety. The mechanism of anxiolytic effect achieved by NAC may include the decline in oxidative damage that down regulates increased apoptosis and reverses the anxiogenic action of cisplatin.

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Section: Discussionmentioning

confidence: 72%

N-Acetylcysteine Protects against the Anxiogenic Response to Cisplatin in Rats

et al. 2019

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“…It was observed in previous studies that MK-801 leads to volumetric shrinkage in the white matter of the brain, and it was found that this shrinkage was caused by degeneration in the neurons and myelin sheaths found in this region (Xiu et al 2014;. In recent years, various studies have revealed that NAC has a protective effect against neurotoxicity and myelin degeneration (Mirzakhani et al 2016;Zaki et al 2018). In the study by Zaki et al (2018), where NAC was applied for protective purposes against cisplatin toxicity, it was reported that the myelin sheath on the sciatic nerve was affected by cisplatin toxicity, this led to folding, dissolution and degeneration in the myelin sheath, whereas NAC had a protective effect in the NAC-given rats, and in these rats, the structure of the myelin sheath was close to that in the control group.…”

Section: Discussionmentioning

confidence: 97%

“…In recent years, various studies have revealed that NAC has a protective effect against neurotoxicity and myelin degeneration (Mirzakhani et al 2016;Zaki et al 2018). In the study by Zaki et al (2018), where NAC was applied for protective purposes against cisplatin toxicity, it was reported that the myelin sheath on the sciatic nerve was affected by cisplatin toxicity, this led to folding, dissolution and degeneration in the myelin sheath, whereas NAC had a protective effect in the NAC-given rats, and in these rats, the structure of the myelin sheath was close to that in the control group. In another study, where Mirzakhani et al (2016) investigated the protective activity of NAC, it was stated that NAC applied on rats whose sciatic nerves were damaged by compression increased the recovery in the sciatic nerves and reduced the negative changes in the myelin sheath.…”

Section: Discussionmentioning

confidence: 99%

“…Other studies have also reported that NAC application showed bene cial outcomes in schizophrenia symptoms (Bulut et al 2009). In toxicological studies conducted on the nervous system, it has been shown that NAC has positive, improving and protective effects against demyelination (Mirzakhani et al 2016;Hichor et al 2018;Zaki et al 2018). Besides, so far, no study has been encountered to examine the effects of NAC on neurotoxicity associated with schizophrenia.…”

Section: Introductionmentioning

confidence: 99%

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The influence of N-Acetylcysteine on locomotor activity, brain oxidative damage, and demyelination in MK-801 model of schizophrenia

Akosmans

Türkmen

Demirel

2021

Preprint

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The purpose of this study is to investigate the effects of N-acetylcysteine (NAC) on potential cerebral demyelination, oxidative damage and schizophrenia-like behaviors caused by MK-801 which is an N-methyl-D-aspartate glutamate receptor antagonist. For this, 4 groups were formed by dividing 24 male BALB/c mice into groups of six. The control group was given a saline solution (10 ml/kg) intraperitoneally (i.p.). While MK-801 (1 mg/kg-i.p.) was given both alone and with NAC (100 mg/kg-i.p.), the last group was given only NAC (100 mg/kg-i.p.). The injections were made for 14 days. It was observed that, MK-801 caused behavioral problems. When the brain was examined, it was determined that it caused a reduction in the weight of the brain, glial cell infiltration, vacuolization in neurons and shrinking in the cell nuclei in the hippocampus. A reduction in myelin basic protein (MBP) secretion was also observed. In the mice given NAC as a protector, it was observed that behavioral problems covered, antioxidant levels increased, and other impairments were repaired. It was concluded that NAC may have a neuroprotective effect.

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“…When NAC is used in hepatic stellate cells (HSCs), it can inhibit hepatic fibrosis and HCC development [114] . Moreover, the use of NAC in HCC mice inhibited the high expression of GST, which may be related to insulin-like growth factor I (IGF-I) and iNOS [115,116] .…”

Section: Natural Anti-inflammatory Agentsmentioning

confidence: 99%

Understanding the inflammation-cancer transformation in the development of primary liver cancer

Chen¹,

Hu²,

Xu³

et al. 2018

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Primary liver cancer is one of the leading causes of cancer-related deaths worldwide. China has more than 55% liver cancer cases globally. The development of hepatocellular carcinoma (HCC) was caused by a variety of risks factors, including chronic inflammation by virus, alcohol consumption and non-alcoholic steatohepatitis. Emerging evidence has notarized inflammation as a critical component of HCC progression. The development of HCC is a multistep process which may originate from liver chronic injury and inflammation to subsequent fibrosis and/or cirrhosis and finally HCC. A large number of studies indicate that chemokines and cytokines are candidates linking molecules between inflammation and liver cancer. Here, we will describe a few of the key cytokines and chemokines and signal pathways which are involved in the inflammation of HCC. Inhibitors of inflammation for the prevention and overcoming antitumor immunity for treatment of liver cancer are promising candidates for the future management of patients with HCC.

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N-acetylcysteine versus progesterone on the cisplatin-induced peripheral neurotoxicity

Abstract: The toxic effect of CIPN might be attributed to either oxidative or severe inflammatory stress. Progesterone is efficient in ameliorating these effects; however, NAC is better. (Folia Morphol 2018; 77, 2: 234-245).

Cited by 21 publications

References 54 publications

N-Acetylcysteine Protects against the Anxiogenic Response to Cisplatin in Rats

N-Acetylcysteine Protects against the Anxiogenic Response to Cisplatin in Rats

The influence of N-Acetylcysteine on locomotor activity, brain oxidative damage, and demyelination in MK-801 model of schizophrenia

Understanding the inflammation-cancer transformation in the development of primary liver cancer

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