N-Acetyl-L-Cysteine for Preventing Lung Reperfusion Injury After Liver Ischemia-Reperfusion

Weinbroum, Avi A.; Rudick, Valery; Ben‐Abraham, Ron; Karchevski, Ela

doi:10.1097/00007890-200003150-00031

Cited by 60 publications

(55 citation statements)

References 25 publications

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“…However, it is also used for the diseases of the lungs, liver, heart, and kidney in order to treat their toxic and ischemic injuries [22][23][24][25] .…”

Section: Discussionmentioning

confidence: 99%

N-acetylcysteine Prevents Gentamicin Ototoxicity in a Rat Model

Somdas¹,

Korkmaz²,

Gürgen³

et al. 2015

Int Adv Otol

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OBJECTIVE:The possible preventive effect of N-acetylcysteine (NAC) in gentamicin ototoxicity was studied with auditory brain stem responses (ABRs), otoacoustic emissions (OAEs), and histopathological investigation of the cochlea. MATERIALS and METHODS:This study is conducted on 36 rats in three groups. Gentamicin, gentamicin plus NAC, and NAC alone were intraperitoneally administered for 15 days. The rats were sacrificed to study the cochleas after testing hearing levels. RESULTS:ABR thresholds and OAEs were attenuated in the gentamicin group, in which apoptosis was detected with histopathological investigation. The group that received NAC in addition to gentamicin had better ABR thresholds and better OAEs. The histopathological evidence of apoptosis in was considerably less in this group. CONCLUSION:Gentamicin ototoxicity can be detected by ABR and OAE testing in rats, and NAC may protect the cochlear cells from apoptosis.

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“…However, it is also used for the diseases of the lungs, liver, heart, and kidney in order to treat their toxic and ischemic injuries [22][23][24][25] .…”

Section: Discussionmentioning

confidence: 99%

N-acetylcysteine Prevents Gentamicin Ototoxicity in a Rat Model

Somdas¹,

Korkmaz²,

Gürgen³

et al. 2015

Int Adv Otol

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“…For the period of reperfusion was chosen by a time of 48 hours long considered when comparing to previous studies, because in short periods is well-known how tecidual injury occurs 4,22,23 .…”

Section: Discussionmentioning

confidence: 99%

“…Its pharmacological effects include suppression of the production of tumor necrosis factor alpha, inhibit platelet aggregation, modulation of cell activation inflammatory 18 . Thus, the hypothesis that NAC acts directly protecting the cell damage may be considered, because the properties attributed to the antioxidant NAC and inhibition of inflammatory processes of lung cells are described in studies at different times of reperfusion and with application prior or during ischemia hepátic 22,[24][25][26] .…”

Section: Discussionmentioning

confidence: 99%

The role of N-acetyl-cysteine in the lung remote injury after hepatic ischemia and reperfusion in rabbits

Castro

Lauz

et al. 2012

Acta Cir. Bras.

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PURPOSE:To study the lesions in the lung of rabbits caused by ischemia/reperfusion hepatic (I/R) after the use of N-acetyl-cysteine (NAC). METHODS: Twenty-four rabbits distributed in two groups: control group GI (n = 12) 5% glucose solution and experiment group GII (n = 12) NAC. The animals were pre-anesthetized with 1% acepromazine maleate and anesthetized with ketamine 10% and 2% xylazine intramuscularly. The GI and GII were given glucose solution intravenously or NAC 15min before occlusion of the hepatic pedicle (30 min). After the period of reperfusion of 24h (n = 6) or 48h (n = 6), liver and lung samples were collected for histology and immunohistochemistry to assess the impairment of cell. RESULTS:The animals of GII and GII-24h-48h showed parenchyma liver close to normal, when using NAC. The GII and GII-24h-48h showed lower thickness of alveolar cells that GI and GI-24h-48h. The expression of caspase 3 in lung cells GII presented smaller value compared to the GI group. CONCLUSION: N-acetyl-cysteine administered 15min prior to the injury ischemia/reperfusion had a significant protective role by minimizing lung injury and apoptotic morphology in the period observed. Key words: Acetylcysteine. Lung. Reperfusion. Ischemia. Liver. Rabbits. RESUMO OBJETIVO:Estudar as lesões no fígado e no pulmão de coelhos, provocadas pela isquemia/reperfusão hepática (I/R) moduladas pelo uso da N-acetil-cisteína (NAC). MÉTODOS: Vinte e quatro coelhos distribuídos em dois grupos: Grupo controle GI (n=12) solução de glicose 5% e Grupo experimento GII (n=12) NAC. Os animais foram pré-anestesiados com maleato de acepromazina 1% e anestesiados com cloridrato de quetamina 10% e xilazina 2% via intramuscular. Os grupos GI e GII receberam solução glicosada ou NAC respectivamente via endovenosa 15min antes da oclusão do pedículo hepático (30 min). Após iniciou-se o período de reperfusão por 24h (n=6) ou 48h (n=6), terminada a reperfusão, amostras do fígado e pulmão foram coletadas para a histologia e imunoistoquímica para avaliar o comprometimento celular. RESULTADOS: Os animais do grupo GII-24h e GII-48h apresentaram arquitetura do parênquima hepático próximo do normal, quando se utilizou NAC. Os grupos GII-24h e GII-48h apresentaram menor espessura das células alveolares que os grupos GI-24h e GI-48h. A expressão da caspase 3 nas células pulmonares do grupo GII, apresentou valor menor comparada ao grupo GI. CONCLUSÃO: A N-acetil-cisteína administrada 15min prévios a lesão da isquemia/reperfusão teve um papel protetor significativo minimizando as lesões morfológicas e apoptóticas pulmonares nos períodos observados. Descritores: Acetilcisteína. Pulmão. Reperfusão. Isquemia. Fígado. Coelhos.

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“…Thus, in the second model, HSA would compete for NO released by activated macrophages, impairing pathological processes requiring high local concentrations of NO or peroxynitrite. Recent in vivo studies have shown that administration of acetylcysteine ameliorates the toxic effects of a variety of experimentally or clinically induced ischemia-reperfusion syndromes of the heart, kidney, lung and liver [2,4,45]. Some have suggested that this protective affect of acetylcysteine may be due to its ability to react with NO.…”

Section: Discussionmentioning

confidence: 99%

Site-Directed Mutagenesis Studies of Human Serum Albumin Define Tryptophan at Amino Acid Position 214 as the Principal Site for Nitrosation

Harohalli

Petersen

et al. 2002

Journal of Biomedical Science

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The patterns of nitric oxide (NO) release from nitrosated bovine serum albumin (BSA), human serum albumin (HSA) and a number of recombinant HSA mutants were compared. All albumin species were nitrosated by incubation with acidified NO₂^–. The pattern of NO release from BSA nitrosated with acidified NO₂^– was in agreement with previous reports which indicated that Cys-34 is the primary target for nitrosation in BSA. In contrast, the pattern of NO release from HSA nitrosated with acidified NO₂^– indicated that the primary nitrosation target was an amino acid residue other than Cys-34. Based on our initial findings and a previous report that tryptophan is a potential target for nitrosation by acidified NO₂^–, several recombinant HSA mutants were synthesized in the yeast species Pichia pastoris. The following recombinant HSA species were produced: wild-type, C34S, W214L, W214E and W214L/Y411W HSA. Nitrosation of these mutants using acidified NO₂^– showed that Trp-214 is the primary nitrosation target in HSA. Mutation of Trp-214 led to an increase in Cys-34 nitrosation, indicating possible competition between these two residues for reaction with N₂O₃, the reactive nitrosating species formed in aqueous acidified NO₂^– solutions.

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N-Acetyl-L-Cysteine for Preventing Lung Reperfusion Injury After Liver Ischemia-Reperfusion

Abstract: Lung treatment with NAC during its reperfusion with IR liver effluent prevented ALI. Lung GSH replenishment accounted for lung protection, but its content did not correlate directly with grade of protection; NAC itself seemingly afforded lung protection as well.

Cited by 60 publications

References 25 publications

N-acetylcysteine Prevents Gentamicin Ototoxicity in a Rat Model

N-acetylcysteine Prevents Gentamicin Ototoxicity in a Rat Model

The role of N-acetyl-cysteine in the lung remote injury after hepatic ischemia and reperfusion in rabbits

Site-Directed Mutagenesis Studies of Human Serum Albumin Define Tryptophan at Amino Acid Position 214 as the Principal Site for Nitrosation

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