N-acetyl-l-cysteine Prevents Bile Duct Ligation Induced Renal Injury by Modulating Oxidative Stress

Sandhir, Rajat; Kaur, Sandeep; Dhanda, Saurabh

doi:10.1007/s12291-016-0627-0

Cited by 7 publications

(4 citation statements)

References 41 publications

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“…Based on these facts and considering its bioavailability and safety, NAC has also been used as an antioxidant in several in vivo studies [5]. In vivo, NAC treatment was found to prevent and/or inhibit the oxidative process as measured by different biomarkers of oxidative stress [11][12][13][14][15][16]. The in vivo antioxidant activity can be explained by considering the antioxidant and radical scavenging mechanism of NAC as observed in in vitro conditions.…”

Section: Introductionmentioning

confidence: 99%

N-Acetylcysteine as an antioxidant and disulphide breaking agent: the reasons why

Aldini

Altomare

Baron

et al. 2018

Free Radical Research

560

433

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The main molecular mechanisms explaining the well-established antioxidant and reducing activity of N-acetylcysteine (NAC), the N-acetyl derivative of the natural amino acid l-cysteine, are summarised and critically reviewed. The antioxidant effect is due to the ability of NAC to act as a reduced glutathione (GSH) precursor; GSH is a well-known direct antioxidant and a substrate of several antioxidant enzymes. Moreover, in some conditions where a significant depletion of endogenous Cys and GSH occurs, NAC can act as a direct antioxidant for some oxidant species such as NO and HOX. The antioxidant activity of NAC could also be due to its effect in breaking thiolated proteins, thus releasing free thiols as well as reduced proteins, which in some cases, such as for mercaptoalbumin, have important direct antioxidant activity. As well as being involved in the antioxidant mechanism, the disulphide breaking activity of NAC also explains its mucolytic activity which is due to its effect in reducing heavily cross-linked mucus glycoproteins. Chemical features explaining the efficient disulphide breaking activity of NAC are also explained.

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Section: Introductionmentioning

confidence: 99%

N-Acetylcysteine as an antioxidant and disulphide breaking agent: the reasons why

Aldini

Altomare

Baron

et al. 2018

Free Radical Research

560

433

View full text Add to dashboard Cite

show abstract

“…Since the 1980s, NAC has been suggested as an antidote in managing maladies associated with oxidative stress in its pathogenesis (Dodd et al., 2008). Several studies have reported NAC effectiveness in mitigating toxicity stemming from oxidative mechanism (Michelucci et al., 2017; Sandhir et al., 2017; Sueishi et al., 2014). NAC thiol moiety is readily bioavailable, relatively stable and safe (Owumi et al., 2015; Zhang et al., 2018) and exhibits beneficial antioxidant tendencies.…”

Section: Discussionmentioning

confidence: 99%

N ‐acetyl cysteine co‐treatment abates perfluorooctanoic acid‐induced reproductive toxicity in male rats

et al. 2021

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Perfluorooctanoic acid is a synthetic perfluoroalkyl—persistent in the environment and toxic to humans. N‐acetylcysteine is a pro‐drug of both amino acid l‐cysteine and glutathione—a non‐enzymatic antioxidant. N‐acetylcysteine serves as an antidote for paracetamol poisoning and alleviates cellular oxidative and inflammatory stressors. We investigated N‐acetylcysteine role against reproductive toxicity in male Wistar rats (weight: 140–220 g; 10 weeks old) posed by perfluorooctanoic acid exposure. Randomised rat cohorts were dosed both with perfluorooctanoic acid (5 mg/kg; p.o) or co‐dosed with N‐acetylcysteine (25 and 50 mg/kg p.o) for 28 days. Sperm physiognomies, biomarkers of testicular function and reproductive hormones, oxidative stress and inflammation were evaluated. Co‐treatment with N‐acetylcysteine significantly (p < .05) reversed perfluorooctanoic acid‐mediated decreases in reproductive enzyme activities, and adverse effect on testosterone, luteinising and follicle‐stimulating hormone concentrations. N‐acetylcysteine treatment alone, improved sperm motility, count and viability, and reduced total sperm abnormalities. Co‐treatment with N‐acetylcysteine mitigated perfluorooctanoic acid‐induced alterations in sperm function parameters. N‐acetylcysteine abated (p < .05) perfluorooctanoic acid‐induced oxidative stress in experimental rats testes and epididymis, and generally improved antioxidant enzyme activities and cellular thiol levels. Furthermore, N‐acetylcysteine suppressed inflammatory responses and remedied perfluorooctanoic acid‐mediated histological injuries in rat. Cooperatively, N‐acetylcysteine enhanced reproductive function in perfluorooctanoic acid dosed rats, by lessening oxidative and nitrative stressors and mitigated inflammatory responses in the examined organ.

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“…Some studies using a BDL adult rat model correlate oxidative stress and generation of free radicals with cirrhosis induced renal damage 25 , 26 . Similarly, changes in the NOS gene expression in the kidneys were observed in our model.…”

Section: Discussionmentioning

confidence: 99%

Cardiac and renal effects of liver cirrhosis in a growing animal model

et al. 2021

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Purpose: To assess the biochemical, histological, histomorphometric and molecular effects of biliary duct ligation (BDL) induced liver cirrhosis in the heart and kidneys. Methods: Thirty-two weaning rats (21 days old, 50-70 g) underwent BDL and were divided in four groups (euthanasia after two, four, six, and eight weeks, respectively) and compared to control groups. Results: The animals' hearts of group 3 were bigger than those of the control group (p=0.042), including thinner right ventricle wall, decreased internal diameter of ventricles, and increased perivascular collagen deposition in left ventricle, as well as increased interstitial collagen in right ventricle after six weeks. In the kidneys of groups 3 and 4, bilirubin impregnation in the tubules, hydropic degeneration, loss of nuclei and lack of plasmatic membrane limits were noted. Nitric oxide synthase (NOS) gene expressions were higher in group 1 (p=0.008), and endothelial nitric oxide synthase (eNOS) gene expressions were elevated in all experimental groups (p=0.008, p=0.001, p=0.022, and p=0.013, respectively). In the heart, a decreased expression of eNOS in group 1 (p=0.04) was observed. Conclusions: Liver cirrhosis leads to histological and histomorphometric alterations in the heart and kidneys, with changes in the NOS and eNOS gene expressions, that may suggest a role in the associated myocardial and renal manifestations.

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N-acetyl-l-cysteine Prevents Bile Duct Ligation Induced Renal Injury by Modulating Oxidative Stress

Cited by 7 publications

References 41 publications

N-Acetylcysteine as an antioxidant and disulphide breaking agent: the reasons why

N-Acetylcysteine as an antioxidant and disulphide breaking agent: the reasons why

N ‐acetyl cysteine co‐treatment abates perfluorooctanoic acid‐induced reproductive toxicity in male rats

Cardiac and renal effects of liver cirrhosis in a growing animal model

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