About the oxidative stress status in children with kwashiorkor

Albrecht, R.; Pélissier, M.A.

doi:10.1016/0278-6915(95)00082-8

Cited by 12 publications

(6 citation statements)

References 22 publications

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“…53 Another explanation may be due to a reduction in CAT synthesis rate as result of dietary restrictions in MN organisms. 54 As mentioned above, t-BHQ is a known Nrf2 inductor, however, contrary to what was expected, no significant differences were found in this transcription factor content in the subcellular fractions analyzed (data not show), probably because Nrf2 distribution in the different cytoplasmic compartments is a fast temporal and spatial event, 55 which did not coincide with our experimental determinations, that were carried out at the end of the treatment.…”

Section: Discussioncontrasting

confidence: 65%

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t-BHQ Protects Against Oxidative Damage and Maintains the Antioxidant Response in Malnourished Rats

et al. 2018

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Objective:Tert-butylhydroquinone (t-BHQ) protective effect against oxidative damage in thymus from malnourished pops-rats was evaluated.Methods:Malnutrition in pops-rats was induced during the lactation period and first-, second-, and third-degree malnourished rats were studied (MN1, MN2, and MN3). To determine t-BHQ protective effect, lipid peroxidation (LPx) was assessed, as well as the carbonyl content. The reduced glutathione and glutathione disulfide content were determined and antioxidant enzyme activities were measured.Results:Oxidative protein damage, LPx, and Nuclear Factor-κB (NF-κB) content, increased in the MN2 and MN3 compared to well-nourished rats, associated with lower protein content and antioxidant activity of superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase. Tert-butylhydroquinone treatment induced a protective effect against lipids and proteins oxidative damage, as well as decrease in NF-κB in MN rats and restored the antioxidant mechanisms, mostly GPx and SOD. No differences were found between male and female animals.Conclusions:Results show that higher body weight deficit leads to increased oxidative damage and probably inflammation, attributable to alterations in antioxidant mechanisms. These effects were reversed by the t-BHQ-treatment, which restores the antioxidant response. Our findings suggest that t-BHQ could be an interesting pharmacological intervention, but it needs to be studied further.

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Section: Discussioncontrasting

confidence: 65%

“…53 Another explanation may be due to a reduction in CAT synthesis rate as result of dietary restrictions in MN organisms. 54 …”

Section: Discussionmentioning

confidence: 99%

t-BHQ Protects Against Oxidative Damage and Maintains the Antioxidant Response in Malnourished Rats

et al. 2018

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“…Protein restriction in rats with type 2 diabetes, cause an accelerated oxidative stress [10,11]. Children with kwashiorkor have a higher level of lipid preoxidation [12][13][14]. Consistently protein malnutrition in intra uterine growth retardation pregnancies is the leading cause of oxidative stress in these patients [15,16].…”

Section: Introductionmentioning

confidence: 99%

Urea and Oxidative Stress in Type 2 Diabetes

Morteza¹,

Jenab²,

Nargesi³

et al. 2012

J Metabolic Synd

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Here we aimed to study the correlation of serum urea as an indicator of protein metabolism with MDA and SOD as markers of oxidative stress in patients with type 2 diabetes. Methods We performed a cross sectional study on 151 patients with type 2 diabetes from the diabetes clinic of Vali Asr hospital affiliated with Tehran University of Medical Science plus 45controls. Diabetes was diagnosed according to the criteria of the American Diabetes Association which is based on glycemia [24]. Exclusion criteria were smoking, pregnancy, creatinine >1.5 mg/dl or GFR< 70 cc/min, glomerulonephritis, thyroid disorders, acute infections, stroke, diabetic ketoacidosis, non-ketonic hyperosmolar diabetes, congestive heart failure, use of antioxidant and hospital admission in recent 6 months. None of the participants were on hormone replacement therapy. Controls were healthy volunteers from the patients' concomitants or hospital staffs. Healthy controls were selected from those without any known disease including type 2 diabetes, hyperlipidemia, ischemic heart disease and malignancy. Demographic and anthropometric data including age, sex, duration of diabetes, height and weight in light clothing and blood pressure in sitting position were recorded. Blood pressure was re measured twice after 5 minutes average. The body mass index (BMI; Kg/m 2) was calculated according to the Quetelet formula. Diet was almost similar in composition in all the studied groups.

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“…Golden and Ramdath (8) hypothesized that cell damage from free radicals leads to edema, fatty infiltration of the liver, and skin lesions in children with kwashiorkor. This theory, however, has not been firmly established or subjected to the test of animal experiments (33). Although the gastrointestinal tract has a particularly enhanced capacity to provide protection against lipid peroxidation (34), our data suggested that the Tbars level increased during the time course of malnutrition.…”

Section: Discussionmentioning

confidence: 67%

Palm Versus Soybean Oil on Intestinal Recovery from Malnutrition in Guinea Pigs

et al. 2002

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Recent recommendations on feeding malnourished children do not provide indication on the nature of dietary lipids. Our aim was to compare the effect of palm oil (mainly saturated and monounsaturated fatty acids) and soybean oil (mainly polyunsaturated fatty acids) on the recovery from malnutrition in guinea pigs. In a first experiment, guinea pigs received a balanced (control group) or a maize (malnourished group) diet for 7, 12, and 21 d. In a second experiment, after 12 d of malnutrition, guinea pigs received a rehabilitation diet containing palm or soybean oil. Both rehabilitation diets allowed a partial recovery from the severe weight loss induced by malnutrition. Thiobarbituric acid reactive substances content, measured in intestinal homogenates, increased in malnourished guinea pigs compared with control animals (40%, p < 0.05) and returned to near control values after rehabilitation with palm (10%) but not soybean (43%) oil diet. Intestinal short-circuit current, assessed in jejunal segments mounted in Ussing chambers, increased progressively during malnutrition (p < 0.001) and returned to near control values with both rehabilitation diets. Compared with control animals, the cell turnover (Ki-67 index assessed by immunohistochemistry detection of the Ki-67 antigen) decreased after soybean (-60%, p < 0.01) but not after palm oil. These results confirm that experimental polydeficient malnutrition induces oxidative stress and dysfunction in the intestine. They show a differential effect of palm and soybean oil on these intestinal measurements, suggesting that the composition of dietary lipids may be important in the treatment of malnutrition.

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About the oxidative stress status in children with kwashiorkor

Cited by 12 publications

References 22 publications

t-BHQ Protects Against Oxidative Damage and Maintains the Antioxidant Response in Malnourished Rats

t-BHQ Protects Against Oxidative Damage and Maintains the Antioxidant Response in Malnourished Rats

Urea and Oxidative Stress in Type 2 Diabetes

Palm Versus Soybean Oil on Intestinal Recovery from Malnutrition in Guinea Pigs

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