Changes in (Na + K)-Adenosine Triphosphatase Activity and Ultrastructure of Lung and Kidney Associated With Oxidative Stress Induced by Acute Ethanol Intoxication

Rodrigo, Ramón; Trujillo, Sergio Hernández; Bosco, Cleofina; Orellana, Myriam; Thielemann, Lilian; Araya, Julia

doi:10.1378/chest.121.2.589

Cited by 46 publications

(24 citation statements)

References 32 publications

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“…It has been demonstrated that oxidative lung injury induced by oleic acid is associated with increases in MDA levels and MPO activity while Na + /K + ATP-ase activity is decreased (37). Similarly, in acute ethanol intoxication the pump activity was also found to be decreased suggesting that oxidative stress plays a role in the maintenance of lung Na + K-ATPase, since GSH depletion seems to be a major determinant of this effect (38). On the other hand, in our study etanercept treatment increased the Na + /K + ATP-ase activity in parallel with a decrease in MDA levels.…”

Section: Discussionmentioning

confidence: 99%

Etanercept protects remote organ damage in a rat model of thermal injury

Şehirli¹

2011

mpj

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Section: Discussionmentioning

confidence: 99%

Etanercept protects remote organ damage in a rat model of thermal injury

Şehirli¹

2011

mpj

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“…Rats in the ethanol group received 2 g/kg ethanol (3 ml) by an intraperitoneal injection (as described by Rodrigo et al [9]). The control rats were given the same amount of 0.9% NaCl.…”

Section: Methodsmentioning

confidence: 99%

Alcohol-Induced Lung Damage and Increased Oxidative Stress

Aytaçoğlu

Çalıkoğlu²,

Tamer³

et al. 2006

Respiration

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Background: Alcohol-induced lung damage may be associated with increased oxidative stress. Objective: Our aim was to investigate alcohol-induced changes in the biochemistry and histopathology of the lung. Methods: Rats were divided into two groups, a control group and an ethanol group. The ethanol group received 2 g/kg ethanol (total: 3 ml) intraperitoneally. The controls were given the same amount of saline via the same route. Three hours later, the rats were sacrificed, and blood and lung tissue samples were obtained. Oxidative stress was assessed by measuring the levels of erythrocyte reduced glutathione (GSH), tissue malondialdehyde (MDA), myeloperoxidase (MPO) and Na⁺-K⁺ ATPase. Histopathologic evaluation of the lung tissues was also performed. Results: In the ethanol group, serum and tissue MDA levels and MPO activities were increased (p = 0.007, p = 0.001 and p = 0.000), and lung tissue Na⁺-K⁺ ATPase activities and erythrocyte GSH were decreased (p = 0.001 and p = 0.000) compared to the controls. Histopathologic examination demonstrated alveolocapillary thickening, alveolar degeneration, leukocyte infiltration and erythrocyte extravasation in the lungs of the ethanol group (p < 0.05). Conclusion: These results suggest that high-doseacute alcohol administration aggravates systemic and local oxidative stress leading to acute lung injury, ranging from mild pulmonary dysfunction to severe lung injury. It should be borne in mind that rapid onset of the acute respiratory distress syndrome (ARDS) may also be due to increased oxidative stress following alcohol abuse, especially when ischemic disturbances, e.g. coronary heart disease, acute ischemia of the extremities and traumatic accidents, are concomitantly present. Therefore, precautions against ARDS may prevent morbidity and mortality in alcohol-induced lung damage in at-risk patients.

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“…11 Oxidative stress-and reactive oxygen species (ROS)-mediated toxicity have been considered the primary routes to alcohol-induced kidney injury. 12,13 Thus, chronic and excessive alcohol consumption may accelerate oxidative mechanism directly or indirectly, which eventually produces cell death and tissue damage. 14 Ascorbic acid (vitamin C) is a low molecular mass antioxidant that interacts directly with the oxidizing radicals and protects the cells from ROS.…”

Section: Introductionmentioning

confidence: 99%

Melatonin and Vitamin C Ameliorate Alcohol-Induced Oxidative Stress and eNOS Expression in Rat Kidney

et al. 2012

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Objectives: The aim of this study was to investigate the preventive effects of melatonin and vitamin C as antioxidants on renal injury in chronic alcohol consumption. Materials and methods: A total of 24 adult male Wistar rats weighing 200-250 g were used in the study. Rats were divided into four equal groups. Group I (control): rats were not fed on alcohol; Group II: rats were fed on alcohol; Group III: rats were fed on alcohol and 40 mg/kg vitamin C; and Group IV: rats were fed on alcohol and 4 mg/kg melatonin. Results: Light microscopic examination revealed atrophic renal corpuscles, dilatation and congestion of the peritubular vessels, and renal corpuscles with obscure Bowman's space and a few foamy-appearing tubules due to alcohol consumption were observed. Expression of endothelial nitric oxide synthase (eNOS) was localized to glomerulus, distal, and collector tubules. eNOS staining decreased in alcohol treatment group and melatonin and vitamin C encore increased expression pattern of eNOS. Alcohol consumption increased malondialdehyde (MDA) level and superoxide dismutase (SOD) and catalase (CAT) activities significantly in the alcohol consumption groups compared with that in the control group, while in melatonin give group just MDA level was decreased statistically significant and SOD and CAT activities were also decreased numerically compared with the alcohol consumption groups. Conclusions: These results indicated that chronic alcohol consumption caused renal damage by increased lipid peroxidation and melatonin and vitamin C administration produced in some degree protection against alcohol-induced damage.

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Changes in (Na + K)-Adenosine Triphosphatase Activity and Ultrastructure of Lung and Kidney Associated With Oxidative Stress Induced by Acute Ethanol Intoxication

Cited by 46 publications

References 32 publications

Etanercept protects remote organ damage in a rat model of thermal injury

Etanercept protects remote organ damage in a rat model of thermal injury

Alcohol-Induced Lung Damage and Increased Oxidative Stress

Melatonin and Vitamin C Ameliorate Alcohol-Induced Oxidative Stress and eNOS Expression in Rat Kidney

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