Antioxidant enzymes and lipoperoxide in blood in uremic children and adolescents

Asayama, Kohtaro; Shiki, Yuji; Ito, Hiroshi; Hasegawa, Osamu; Miyao, Akiyo; Hayashibe, Hidemasa; Dobashi, Kazushige; Kato, Kiyohiko

doi:10.1016/0891-5849(90)90112-v

Cited by 47 publications

(21 citation statements)

References 22 publications

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“…Although the possibility remains that the lipid peroxide detected in the plasma was derived from other organs, the present results do not support the existence of enhanced oxidative stress and subsequent oxidative injury to the organs studied. The observed significant correlations between plasma lipids and plasma TBARS were found previously in other clinical models [19]. A larger amount of lipid substrate provided by hyperlipidemic plasma may increase de novo lipid peroxidation during incubation in the assay system, thereby resulting in an apparent elevation in the plasma TBARS levels.…”

Section: Discussionsupporting

confidence: 69%

Lipid peroxidation and antioxidant enzyme status in various tissues of mice with gold-thioglucose-induced obesity.

Asayama

Hayashibe

Dobashi

et al. 1990

J. Clin. Biochem. Nutr.

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SummaryTo determine whether an oxidant-antioxidant imbalance exists in the non-genetic obese model, we induced obesity in 3-week-old female ICR mice by gold-thioglucose administration, and the lipid peroxide level and activities of antioxidant enzymes were measured in the plasma, liver, heart, and skeletal muscle. Two types of superoxide dismutase were assayed by radioimmunoassays. Lipid peroxide was estimated from fluorimetric measurement of thiobarbituric acid-reactive substances (TBARS). The plasma levels of both cholesterol (Chol) and triacylglycerol (TG) and liver TG content were increased in the obese mice. The superoxide dismutases were unaltered, while the activities of both glutathione peroxidase and catalase in the obese liver and heart were decreased. Lipid peroxide levels were unaltered in the obese liver and heart, decreased in the skeletal muscle, and increased in the plasma. The body weight correlated positively with the liver weight, heart weight, liver TG, liver Chol, plasma TG, plasma Chol, and plasma TBARS, and inversely with the tissue levels of some of the antioxidant enzymes and TBARS. The tissue levels of the antioxidant enzymes and TBARS had a general tendency to decrease in the obese animals. These results suggest that oxidative stress is enhanced only in the plasma of the obese mice and not in any of the tissues studied here. lism produces an accumulative deleterious change in mitochondrial function at a rate related to the rate of oxygen consumption, leading to the aging of the cells [1]. According to this hypothesis, food restriction decreases oxygen consumption, and, in turn, free radical production, resulting in a decreased rate of progression of degenerative disorders including lipid peroxidation [2]. We previously demonstrated that prolonged fasting suppressed mitochondrial oxidative metabolism and lipid peroxidation in certain rat tissues [3]. Conversely, increased food consumption accompanying obesity can enhance oxidative stress, thereby accelerating the degeneration process. Obesity is known to be an independent risk factor of atherosclerosis [4], and the latter process is postulated to be accelerated by an increase in the level of circulating lipid peroxides [5]. Thus, study of the oxidant-antioxidant balance in obesity is of clinical importance. However, little is known about the oxidantantioxidant status in obesity, and data are limited to the genetically obese ob/ob mouse [6][7][8][9]. Abnormal metabolism of trace metals, which is not directly linked to excessive weight gain, is reported to exist in the ob/ob mouse [10]. Such deviation in trace metal status per se may modify tissue levels of antioxidant enzymes, which contain trace metals in their active centers, independently of energy metabolism.To determine whether an oxidant-antioxidant imbalance exists in the nongenetic model of obesity, the obese condition was induced by gold-thioglucose administration to mice, and the lipid peroxide level and activities of antioxidant enzymes were measured in various tissues. MATERI...

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Section: Discussionsupporting

confidence: 69%

Lipid peroxidation and antioxidant enzyme status in various tissues of mice with gold-thioglucose-induced obesity.

Asayama

Hayashibe

Dobashi

et al. 1990

J. Clin. Biochem. Nutr.

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“…For example, anti oxidant enzyme activities were found decreased in uremic red blood cells from the patients with CRF in a study carried out by Turi et al [25]. In another study by Asoyama et al [26], however, it was reported that SOD, GSH-Px and CAT activities in erythrocytes were unaltered in the uremic children maintained on HD and CAPD. On the other hand, Paul et al [24] indicated that plasma and erythrocyte antiox idant capacity of the patients undergoing regular dialysis treatment were significantly decreased and free radical reaction products such as malonyldialdehyde were signifi cantly increased in chronic uremic patients.…”

Section: Discussionmentioning

confidence: 82%

Reduced Erythrocyte Defense Mechanisms against Free Radical Toxicity in Patients with Chronic Renal Failure

Durak¹,

Akyol²,

Başeşme

et al. 1994

Nephron

104

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In this study, activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) enzymes were determined in the erythrocytes from patients with chronic renal failure (CRF) and from healthy subjects. In the conservative drug management group and intermittent ambulatory peritoneal dialysis group, CAT activity was lower than in the control group. However, SOD and GSH-Px activities of these groups were not statistically different from the control values. In the continuous ambulatory peritoneal dialysis group and the hemodialysis group, SOD, GSH-Px and CAT activities were lower than control values. In the patient groups, correlation coefficients between the enzyme activities were also found to be different from the control values. Results suggested that enzymatic antioxidant defense mechanisms were suppressed in the erythrocytes from the patients with CRF, in particular in the erythrocytes from those who were under hemodialysis and continuous ambulatory peritoneal dialysis management. It is proposed that reduced antioxidant defense mechanisms in the erythrocytes is one of the important factors leading to peroxidation in the membrane lipid structure of the erythrocytes and thereby to hemolysis and anemia in the patients with CRF.

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“…Alguns autores têm observado que o estresse oxidativo induz a atividade da SOD em leucócitos e eritrócitos 40 .…”

Section: Arjunclassified

The role of oxidative stress in inflammation in patients with juvenile rheumatoid arthritis

Ramos¹,

Ramos²,

Dominguez³

2000

J Pediatr (Rio J)

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Objective: To determine the level of cellular oxidative stress blood markers and the enzymatic system of antioxidant defense establishing the oxidative profile in patients with Juvenile Rheumatoid Arthritis.Methods: Case-control study that included 64 patients (46 of female sex) with Juvenile Rheumatoid Arthritis (JRA) following clinical control in the Pediatric Rheumatology Service of the Vall d'Hebron Hospital, Barcelona, Spain. The patients were separated in three subtypes based on the pattern of onset within the first six months of disease: polyarticular, pauciarticular and systemic. The control group included 60 patients (38 of female sex) following clinical control to diseases of non inflammatory nature, in the same hospital. The plasmatic levels of malondialdehyde (MDA), lipoperoxide (LPO), hydroperoxide (HPX), carbonile groups (CG) of proteins and gluthathione and the enzymatic activities of Superoxide dismutase (SOD), gluthathione peroxidase (GSH-Px) and gluthathione reductase were determined.Results: The group of patients with JRA presented high concentrations of lipid peroxidation products, evaluated by determining the plasmatic levels of MDA, LPO, and HPX; oxidative damage of the circulate protein, determined by CG contents of plasma proteins; elevation of enzymatic activity of SOD and GSH-Red; decrease of GSH-Px activity and GSH levels.Conclusions: Our results show the presence of molecular damage determined by oxygen free radicals in the JRA patients. The SOD activity and the changes of gluthathione redox enzymatic cycle confirm the decrease of capacity of cellular defense system against the induced toxicity of oxidative stress in these patients. Resultados: Comparados aos controles, os pacientes portadores de ARJ apresentaram concentrações elevadas dos produtos derivados da lipoperoxidação, avaliada pela determinação dos níveis plasmáticos do MDA, HPX e LPO; dano oxidativo das proteínas circulantes, determinado pelo conteúdo de GC de proteínas plasmá-ticas; elevação da atividade enzimática da SOD e GSH-Red; e diminuição da atividade da GSH-Px e dos níveis do GSH. J. pediatr. (Rio J.Conclusões: Estes resultados demonstram a presença de dano molecular determinado pelos radicais livres de oxigênio em pacientes com ARJ. A atividade da SOD e as alterações do ciclo enzimático glutatião-redox confirmam uma diminuição da capacidade dos sistemas de defesa intracelular contra a toxicidade induzida pelo estresse oxidativo nestes pacientes. Introdução A geração de radicais livres ocorre como parte do processo fisiológico do metabolismo aeróbico, secundária à produção de radicais reativos de oxigênio. Desse modo, o metabolismo celular produz radicais livres em condições fisiológicas, e estes radicais ativos podem ter vários efeitos J. pediatr. (Rio J.

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Antioxidant enzymes and lipoperoxide in blood in uremic children and adolescents

Cited by 47 publications

References 22 publications

Lipid peroxidation and antioxidant enzyme status in various tissues of mice with gold-thioglucose-induced obesity.

Lipid peroxidation and antioxidant enzyme status in various tissues of mice with gold-thioglucose-induced obesity.

Reduced Erythrocyte Defense Mechanisms against Free Radical Toxicity in Patients with Chronic Renal Failure

The role of oxidative stress in inflammation in patients with juvenile rheumatoid arthritis

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