Apolipoprotein E deficiency promotes increased oxidative stress and compensatory increases in antioxidants in brain tissue

Shea, Thomas B.; Rogers, Eugene; Ashline, David J.; Ortiz, Daniela; Sheu, Min‐Shyan

doi:10.1016/s0891-5849(02)01001-8

Cited by 105 publications

(73 citation statements)

References 59 publications

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“…In recent years, several polymorphisms playing a role in the development and progression of atherosclerosis have been identified in relation to blood coagulation, endothelial function, and lipid metabolism (75), as is the case of apo E. The serum cholesterol concentration is in part determined by the common apo E polymorphism and the ε4 allele appears to be associated with elevated serum cholesterol concentration (6,(76)(77)(78) and to contribute to an increased risk for coronary artery disease and atherosclerosis (37,79,80). In this study, the high-risk genotypes for atherogenesis (ε3/ε4 and ε4/ε4) were found in a higher percentage in patients, similarly to results of Stengard et al (81,82) and to those of Pirim et al (83).…”

Section: Variations In Apo E Polymorphismmentioning

confidence: 99%

Systemic Markers of the Redox Balance and Apolipoprotein E Polymorphism in Atherosclerosis: The Relevance for an Integrated Study

Lopes

Napoleão

Pinheiro

et al. 2006

BTER

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H u m a n a J o u r n a l s . c o mS e a r c h , R e a d a n d D o w n l o a d Featured in this issue: ABSTRACTProspective studies have demonstrated that an imbalance between oxidative damage and antioxidative protection can play a role in the development and progression of atherosclerosis. Also, genotypes with the apolipoprotein E ε4 allele have been associated with an increase risk for this pathology. Based on this knowledge, the aim of this study was to evaluate indicators of the redox balance, trace elements, and apolipoprotein E allelic profile in subjects from the Lisbon population with clinically stable atherosclerosis, at risk for atherosclerotic events, and in healthy subjects for comparison. The activities of superoxide dismutase in erythrocytes and glutathione peroxidase in whole blood, plasma total thiols, and serum ceruloplasmin were kept unchanged among the three groups. Serum α-tocopherol was increased in atherosclerotic patients. *Author to whom all correspondence and reprint requests should be addressed.lipid and protein oxidative damage, respectively, reached their highest values in risk subjects. The concentrations of potassium and calcium, in plasma and in blood cells, were slightly elevated in patients and might reflect an electrolytic imbalance. Regarding the apolipoprotein E polymorphism, atherosclerotic patients had an increased incidence of the high-risk genotypes for atherogenesis (ε3/ε4 and ε4/ε4). A multivariate model applied to the general population using most of the parameters clearly separated the three groups at study (i.e., the healthy group from the steady-state group of risk disease and from the atherosclerotic one). As shown by us, the usefulness of biochemical and complementary genetic markers is warranted for a better knowledge on atherosclerosis molecular basis.

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Section: Variations In Apo E Polymorphismmentioning

confidence: 99%

Systemic Markers of the Redox Balance and Apolipoprotein E Polymorphism in Atherosclerosis: The Relevance for an Integrated Study

Lopes

Napoleão

Pinheiro

et al. 2006

BTER

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“…In vitro studies have indicated that apoE yields isoform-dependent protection against oxidative insult (Miyata and Smith 1996;Lee et al 2004) and can influence nitric oxide production by microglia in an isoform-dependent manner (Colton et al 2002(Colton et al , 2004. Moreover, when compared with wild-type mice, apoE-deficient mice exhibit increased protein and lipid oxidative damage in several brain regions, decreased endogenous antioxidants, and increased sensitivity to oxidative stress (Shea et al 2002;Veinbergs et al 2000;Choi et al 2004;Matthews and Beal 1996;Ramassamy et al 2001;Montine et al 1999;Reich et al 2001).…”

Section: Introductionmentioning

confidence: 99%

Lifelong vitamin E intake retards age-associated decline of spatial learning ability in apoE-deficient mice

McDonald

Forster

2005

AGE

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The potential for lifelong vitamin E supplementation to delay age-associated cognitive decline was tested in apoE-deficient and wild-type C57BL/6 mice. Beginning at eight weeks of age, the mice were maintained on a control diet or diets supplemented with DL-a-tocopheryl acetate yielding approximate daily intakes of either 20 or 200 mg/kg body weight. When 6 or 18 months of age, cognitive functioning of the mice was assessed using swim maze and discriminated avoidance testing procedures. For the mice maintained on control diets, the agerelated declines in swim maze performance were relatively larger in apoE-deficient mice when compared with wild-type. On the other hand, age-associated declines in learning and working memory for discriminated avoidance were similar in the two genotypes. The 200-mg/kg dose of vitamin E prevented the accelerated decline in spatial learning apparent in 18-month-old apoE-deficient mice, but had no equivalent effect on performance declines attributable to normal aging in the wild-type mice. Vitamin E supplementation failed to prevent agerelated impairments in learning and memory for discriminated avoidance observed in both the wild-type and apoE-deficient mice. The current findings are consistent with the hypothesis that apoE deficiency confers an accelerated, though probably selective, loss of brain function with age. This loss of function would appear to involve pathogenic oxidative mechanisms that can be prevented or offset by antioxidant supplementation.

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“…This may be associated with repair of the immune system. The difference between ALT and AST may be due to the different half-life (19).…”

Section: Discussionmentioning

confidence: 99%

Expression of glutathione S-transferase A1, a phase II drug-metabolizing enzyme in acute hepatic injury on mice

Liu

et al. 2017

Experimental and Therapeutic Medicine

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Abstract. In the present study, three models of acute liver injury in mice were induced via the administration of CCl 4 (35 mg/kg, 24 h), acetyl-para-aminophenol (APAP; 200 mg/kg, 12 h) and ethanol (14 ml/kg, 8 h) to study the effect of glutathione S-transferase A1 (GSTA1) on acute liver injury. The serum levels of alanine transaminase, aspartate transaminase and liver homogenate indicators (superoxide dismutase, glutathione and glutathione peroxidase) were significantly lower in model groups compared with the control group (P<0.01), whereas the liver homogenate indicator malondialdehyde was significantly increased (P<0.01). The expression of GSTA1 in liver was significantly decreased in the model groups compared with the control group (P<0.01). GSTA1 protein content was 3.8, 1.3 and 2.6 times lower in the CCl 4, APAP and ethanol model groups, respectively. Furthermore, GSTA1 mRNA expression levels decreased by 4.9, 2.1 and 3.7 times in the CCl 4, APAP and ethanol model groups, respectively. Among the three models, the injury induced by CCl 4 was the most marked, followed by ethanol and finally APAP. These results suggest that GSTA1 may be released by the liver and serve as an antioxidant in the prevention of liver damage. IntroductionLiver disease poses a serious threat to human health and food safety, as consumption of animals with liver disease may be detrimental to health (1). Acute liver injury is the common pathway and initiating factor of many liver diseases, such as acute liver failure (2). Three models of liver injury are typically used in research as they are representational and reflect the situation of hepatotoxicity comprehensively and intuitively (3). CCl 4 is a classical hepatotoxicant, which is able to induce reactive oxygen formation and deplete glutathione (GSH) (4). Acetyl-para-aminophenol (APAP) hepatotoxicity is induced by the electrophile N-acetyl-p-benzoquinoneimine (NAPQI), which is able to induce mitochondrial dysfunction and oxidative stress, leading to liver damage (5). The major etiological factors of hepatotoxicity in ethanol-induced hepatic injury are oxidative stress and inflammatory responses (6). Due to the complexity of liver function and the diversity of liver damage factors, experimental animal models are not able to accurately and fully reflect the nature of liver injury (7). Furthermore, existing animal models have various limitations such as non-standardized methods, lack of reproducibility and non-unified methods (8).Glutathione S-transferases (GSTs) are enzymes that are able to protect cells from damage caused by reactive oxygen species (9). GSTA (α class GST) serves an important cytoprotective role in detoxifying reactive electrophiles and products of lipid peroxidation (10). GSTs including GSTA have previously been identified as inhibitors of stress-activated kinase activity, most notably c-Jun N-terminal kinase (11). This suggests that altered GST expression may be an important factor in modulating the cellular transition between proliferation, differentiation, and apo...

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Apolipoprotein E deficiency promotes increased oxidative stress and compensatory increases in antioxidants in brain tissue

Cited by 105 publications

References 59 publications

Systemic Markers of the Redox Balance and Apolipoprotein E Polymorphism in Atherosclerosis: The Relevance for an Integrated Study

Systemic Markers of the Redox Balance and Apolipoprotein E Polymorphism in Atherosclerosis: The Relevance for an Integrated Study

Lifelong vitamin E intake retards age-associated decline of spatial learning ability in apoE-deficient mice

Expression of glutathione S-transferase A1, a phase II drug-metabolizing enzyme in acute hepatic injury on mice

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