Lipoperoxidation in human and rat brain tissue: Developmental and regional studies

Boehme, D; Kosecki, R.; Carson, SA; Stern, F.; Marks, Neville

doi:10.1016/0006-8993(77)90127-5

Cited by 59 publications

(14 citation statements)

References 17 publications

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“…Two-milliliter samples were withdrawn from the beakers at timed intervals and the TBA assay was carried out as previously described (15,32). Concentration of the tissue homogenate (33 mg/ml) and pH of the TBA assay mixture (7.6) were adjusted to ensure optimal sensitivity and linear concentration dependence (32).…”

Section: Methodsmentioning

confidence: 99%

“…Concentration of the tissue homogenate (33 mg/ml) and pH of the TBA assay mixture (7.6) were adjusted to ensure optimal sensitivity and linear concentration dependence (32). The uncorrected absorbance measurements at 532 nm indicate total TBA-reacting material (TBARM).…”

Section: Methodsmentioning

confidence: 99%

“…After the zero-time sample had been taken, the beakers were incubated at 37°C in a rotary water bath oscillating at 200 rpm. The water bath was covered with a lid and fresh water-saturated air was circulated within the incubator to maintain a constant concentration of oxygen in the incubator and prevent sample evaporation.Two-milliliter samples were withdrawn from the beakers at timed intervals and the TBA assay was carried out as previously described (15,32). Concentration of the tissue homogenate (33 mg/ml) and pH of the TBA assay mixture (7.6) were adjusted to ensure optimal sensitivity and linear concentration dependence (32).…”

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confidence: 99%

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Peroxide-producing potential of tissues: inverse correlation with longevity of mammalian species.

Cutler¹

1985

Proc. Natl. Acad. Sci. U.S.A.

107

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Peroxidation reactions may cause many of the dysfunctions associated with aging. Accordingly, the 30-fold differences in aging rate among the mammalian species could be determined in part by peroxidation defense processes. This possibility was tested by measuring the spontaneous autoxidation of aerobically incubated brain and kidney tissue homogenates of 24 different mammalian species as a function of their maximum lifespan potential. Results show a statistically significant inverse correlation between both the rate of autoxidation and the amount of peroxidizable substrate with maximum lifespan potential. Kinetic analysis of the data indicates that the amount of peroxidizable substrate was the major factor determining the rate of autoxidation. For human tissues, antioxidants also appear to contribute to their unusually low sensitivity to peroxidation. These results support the hypothesis that aging may be caused in part by oxygen radicals initiating peroxidation reactions and that peroxidation defense processes are involved in governing the longevity of mammalian species.Much evidence now supports oxygen radicals as a causative factor in a number of pathologies (1-4), but their importance to aging has largely been based on circumstantial evidence (5-8). Past work in our laboratory has shown a positive correlation in the concentration of a number of different antioxidants per specific metabolic rate with the maximum lifespan potential of mammalian species. These results suggested the potential importance of antioxidants in governing aging rate. However, negative or no correlations with some antioxidants were also found (7, 9, 10). Because of the difficulties in determining the total defense these antioxidants were contributing, a method was needed to estimate the net sensitivity a tissue has against oxidative damage.Aerobically incubated tissue homogenates spontaneously undergo autoxidation (11-15). The rate and extent of this reaction depends upon factors affecting its initiation, propagation, and termination (16-19). Much evidence also indicates that the sensitivity of tissue homogenates to autoxidation in vitro reflects their normal in vivo sensitivity to similar oxidative processes (20-26). Thus, a measure of the autoxidation of aerobically incubated tissue homogenates appears to represent one means of assessing a complex array of tissue defenses against oxygen radicals that may be important in governing the aging rate of different mammalian species. MATERIALS AND METHODSSource of Tissues. Tissues were from Yerkes Regional Primate Center, Duke University Primate Facility, the Washington Regional Primate Center, and Pel-Freez Biologicals. Peromyscus maniculatus (deer mouse), Peromyscus leucopus (white-footed mouse), and Mus musculus (field mouse) were from our own animal colony.Estimation of Species Longevity. Maximum lifespan potentials (MLSPs) are from a literature survey covering over 100 zoos world-wide (27). From these data, mean ± SD values were calculated. Lifespan energy potential (LEP, kcal/g)...

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Peroxide-producing potential of tissues: inverse correlation with longevity of mammalian species.

Cutler¹

1985

Proc. Natl. Acad. Sci. U.S.A.

107

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“…Lipid peroxidation was estimated from the formation of MDA which, together with TBA, forms a colored product (34). Most of the MDA measured in the TBA test is formed from fragmentation of lipid peroxides during incubation at 37°C in the presence of ascorbic acid and an iron salt.…”

Section: Methodsmentioning

confidence: 99%

Lipid Peroxidation and Superoxide Dismutase-1 and Glutathione Peroxidase Activities in Trisomy 16 Fetal Mice and Human Trisomy 21 Fibroblasts

Annerén

Epstein

1987

Pediatr Res

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ABSTRACT. An increase in lipid peroxidation has been reported in fetal human trisomy 21 brains. To determine whether this change can be regarded as a consequence of the increase in soluble Cu, Zn-superoxide dismutase (SOD-1) activity caused by the trisomy, we have made use of the trisomy 16 mouse, a model for human trisomy 21. Lipid peroxidation, as malonaldehyde, and the activities of SOD-1 and glutathione peroxidase were studied in diploid and trisomy 16 mouse fetuses and fetal brains and, for comparison, in diploid and trisomy 21 human fibroblasts. SOD-1 activity in diploid mouse brain increased during fetal and postnatal development, but glutathione peroxidase activity was unchanged. Mean SOD-1 activity was almost exactly 50% increased in trisomy 16 fetuses and fetal brains and in human trisomy 21 fibroblasts, confirming the gene dosage effect in both species. The SOD-1 activity in the trisomic fetuses was correlated with that in their matched diploid littermates, suggesting that factors other than the gene dosage also determine activity. Mean glutathione peroxidase activity was not increased in trisomy 16 fetuses or brains and only slightly increased in human trisomy 21 fibroblasts. Mean lipid peroxidation was decreased in fetal trisomy 16 brains but was increased in human trisomy 21 fibroblasts. These results do not lend support to the notion that increased SOD-1 activity is developmentally deleterious and necessarily increases lipid peroxidation and, secondarily, the activity of glutathione peroxidase. The difference between the human and mouse data concerning lipid peroxidation in trisomic brains may be related to structural differences in the lipids which provide the substrate for lipid peroxidation. (Pediatr Res 21: 88-92,1987) Abbreviations DS, Down syndrome SOD-1, soluble superoxide dismutase, Cu, Zn-superoxide dismutase GSH-Px, glutathione peroxidase

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“…Disodium citrate (3.89%) was used as an anticoagulant. As a measure of lipid peroxidation, malonaldialdehyde formation was estimated, using the level of TBARS, according to the method of Bohme et al [10]. Equal volumes 120 μl of EDTA (10 mM), ascorbate (10 mM), and mixture of EDTA (16.7 mM) and FeSo 4 (16.7 mM) were mixed and to this, platelet suspension (840 μl) was added.…”

Section: Assay Of Lipid Peroxidationmentioning

confidence: 99%

Elevated lipid peroxides induced angiogenesis in proliferative diabetic retinopathy

Saxena

Srivastava²,

Khanna

2010

j ocul biol dis inform

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Oxidative stress is associated with causation of diabetic vascular complications. A case-control study was undertaken to evaluate the association of platelet thiobarbituric acid reacting substances (TBARS) with the severity of diabetic retinopathy for the first time. Platelet TBARS levels were estimated using standard protocol. Platelet TBARS levels in the cases with non-proliferative diabetic retinopathy, proliferative diabetic retinopathy, and healthy controls were 0.56±0.09, 0.69±0.11 and 0.41±0.1 nmol/h/ 10 8 platelets, respectively. A significant increase in platelet TBARS levels was observed in the cases as compared to controls (p<0.001). Elevated TBARS levels were observed to significantly increase further during the proliferative stage of the disease (p<0.01). The increase in platelet TBARS levels, and thereby at retinal level, is associated with angiogenesis in diabetic retinopathy. Supplemental anti-oxidant therapy in diabetic retinopathy may prevent ocular angiogenesis resulting as a consequence of oxidative stress.

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Lipoperoxidation in human and rat brain tissue: Developmental and regional studies

Cited by 59 publications

References 17 publications

Peroxide-producing potential of tissues: inverse correlation with longevity of mammalian species.

Peroxide-producing potential of tissues: inverse correlation with longevity of mammalian species.

Lipid Peroxidation and Superoxide Dismutase-1 and Glutathione Peroxidase Activities in Trisomy 16 Fetal Mice and Human Trisomy 21 Fibroblasts

Elevated lipid peroxides induced angiogenesis in proliferative diabetic retinopathy

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