Thiobarbituric acid reactive substances are increased in the subcutaneous fat tissue of patients with end-stage renal disease

Gotoh, Michihiro; Nagase, Sohji; Aoyagi, Kazumasa; Hirayama, Aki; Takemura, Katsumi; Ueda, Atsushi; Tomida, Chie; Kikuchi, Hiroshi; Kôyama, Akio

doi:10.1093/ndt/12.4.713

Cited by 30 publications

(18 citation statements)

References 8 publications

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“…Our previous report [2]showed that serum antioxidant activity measured as serum scavenging activity against the hydroxyl radical was decreased in uremic plasma, and this was improved by HD. Moreover, we have shown a tendency for TBARS in subcutaneous fat tissue to decrease after the induction of maintenance HD [5]. From the combination of these results, we conclude that a single session of HD does not influence lipid peroxidation of uremic patients.…”

Section: Discussionmentioning

confidence: 78%

“…A previous study from our group using electron spin resonance indicated that the serum antioxidant activity against the hydroxyl radical is decreased in hemodialysis (HD) patients [2]. We have also demonstrated an improvement in the inhibitory effect of serum on the generation of lipid peroxides in hepatic microsomal NADPH-dependent P-450 reductase [3, 4]and an accumulation of thiobarbituric acid reactive substances (TBARS) in subcutaneous fat tissue in end-stage renal disease (ESRD) patients [5]. …”

Section: Introductionmentioning

confidence: 99%

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Hemodialysis Does Not Influence the Peroxidative State Already Present in Uremia

Hirayama

Nagase

Gotoh

et al. 2000

Nephron

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Hemodialysis (HD) patients are exposed to high oxidative stress, however, the nature of this stress is still unclear. In this study, we employed a specific lipid peroxidative product, phosphatidylcholine hydroperoxide (PCOOH), and evaluated the peroxidative effect of end stage renal disease by measuring thiobarbituric acid reactive substances (TBARS) and PCOOH in both plasma and erythrocyte membrane. We also surveyed plasma TBARS and PCOOH before and after HD sessions thereby assessing oxidative stress by a single HD procedure. The plasma TBARS level of healthy controls was 2.9 ± 0.4 nmol/ml. Those of HD patients before and after HD session were 5.1 ± 1.4 and 3.1 ± 0.5 nmol/ml, respectively, and the pre-HD plasma TBARS levels were significantly higher than those of controls and after HD. The Plasma PCOOH concentration of patients before HD was 119.7 ± 58.4 pmol/ml and was significantly higher than that of controls which was 88.6 ± 14.3 pmol/ml. After HD, the plasma PCOOH level decreased to 103.2 ± 36.0 pmol/ml, which was still significantly higher than that of controls. In erythrocytes, the PCOOH level of patients was 259.3 ± 105.4 nmol/g RBC and was significantly higher than that of controls with 88.6 ± 32.0 nmol/g RBC. Analyzed with respect to the cause of renal disease, the polycystic kidney disease patients showed significantly lower plasma PCOOH levels than the others. These results suggest that there is an increase of lipid peroxidation in both plasma and erythrocytes of HD patients, though this oxidative stress was not brought about by HD.

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Section: Discussionmentioning

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Hemodialysis Does Not Influence the Peroxidative State Already Present in Uremia

Hirayama

Nagase

Gotoh

et al. 2000

Nephron

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“…Lipid and protein oxidative markers (TBARS, PC) were significantly increased in HD patients compared to HC. Previous studies have also reported elevated plasma concentrations of lipid peroxidation byproducts and oxidative protein damage in HD patients compared to healthy controls [30,31,32]. In HD patients, lipid peroxidation may be attributed to the formation of advanced glycation end products, even at normal glucose levels [32].…”

Section: Discussionmentioning

confidence: 99%

Acute Exercise May Exacerbate Oxidative Stress Response in Hemodialysis Patients

et al. 2008

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Background/Aims: Hemodialyzed patients (HD) demonstrate elevated oxidative stress (OXS) levels. Exercise effects on OXS response and antioxidant status of HD was investigated in the present study. Methods: Twelve HD and 12 healthy controls (HC) performed a graded exercise protocol. Blood samples, collected prior to and following exercise, were analyzed for lactate, thiobarbituric acid-reactive substances (TBARS), protein carbonyls (PC), reduced (GSH) and oxidized glutathione (GSSG), total antioxidant capacity (TAC), catalase, and glutathione peroxidase (GPX) activity. Results: HC demonstrated higher time-to-exhaustion (41%), lactate (41%) and VO_{2 peak} (55%) levels. At rest, HD exhibited higher TBARS, PC, and catalase activity values and lower GSH, GSH/GSSG, TAC, and GPX levels. Although exercise elicited a marked change of OXS markers in both groups, these changes were more pronounced (p < 0.05) in HD patients. After adjusting for VO_{2 peak}, differences between groups disappeared. VO_{2 peak}was highly correlated with GSH/GSSG, TBARS, TAC and PC at rest and after exercise. Conclusions: These results imply that HD demonstrate higher OXS levels and a lower antioxidant status than HC at rest and following exercise. Acute exercise appears to exacerbate OXS response in hemodialyzed patients probably due to diminished antioxidant defense. However, aerobic capacity level seems to be related to OXS responses in this population.

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“…Few studies have shown the beneficial effect of vitamin E administration on hemodialysis patients [25], which would occur by lowering the lipid peroxide level, whose elevation was shown to be involved in a variety of diseases [26] including end-stage renal disease. Treatment with citrate has been advocated in patients with hypocitraturia because of its lowering effect on calcium oxalate supersaturation by binding calcium [27].…”

Section: Resultsmentioning

confidence: 99%

Effect of Oral Supplementation of Vitamin E on Urinary Risk Factors in Patients with Hyperoxaluria.

Anbazhagan

Hariprasad

Samudram

et al. 1999

J. Clin. Biochem. Nutr.

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SummaryThe effects of administration of vitamin E on hyperoxaluria, hypercalciuria, hyperuricosuria, and hypocitraturia and on the decreased levels of antioxidants such as ascorbic acid, vitamin E, glutathione (GSH), and superoxide dismutase (SOD) in kidney stone patients were observed. Following the surgical removal of kidney stones from the patients, vitamin E (200 mg/day) was administered from the 7th day onwards to twenty patients for up to 90 days. The normalization process of urinary risk factors and antioxidants was rapid in the vitamin E-administered patients when compared with that in the untreated group. The increased excretion of citrate following vitamin E administration was suggested to reduce the retention of calcium oxalate crystals and thereby lower the rate of recurrence of stones. Kidney stone disease is multifarious in origin and the precise mechanism by which kidney stones originate is still not well understood. The relationship between the concentrations of the precipitating substances in urine and the solubility of the salt to be formed [1], the role of nucleating substances [2] , the role of crystal aggregation [3], and the part played by inhibitors of crystal formation and aggregation [4] have been a focus of several workers, and renal injury is considered as one of the prerequisites for calcium oxalate retention [5].

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Thiobarbituric acid reactive substances are increased in the subcutaneous fat tissue of patients with end-stage renal disease

Abstract: This study supports the finding of a severe peroxidative state in patients with end-stage renal disease.

Cited by 30 publications

References 8 publications

Hemodialysis Does Not Influence the Peroxidative State Already Present in Uremia

Hemodialysis Does Not Influence the Peroxidative State Already Present in Uremia

Acute Exercise May Exacerbate Oxidative Stress Response in Hemodialysis Patients

Effect of Oral Supplementation of Vitamin E on Urinary Risk Factors in Patients with Hyperoxaluria.

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