Oxidative reactive species in cell injury - Mechanisms in diabetes mellitus and therapeutic approaches

被引:87
作者
Fridlyand, Leonid E. [1 ]
Philipson, Louis H. [1 ]
机构
[1] Univ Chicago, Dept Med, Chicago, IL 60637 USA
来源
CELL INJURY: MECHANISMS, RESPONSES, AND REPAIR | 2005年 / 1066卷
关键词
beta-cell; insulin resistance; mitochondria; diabetes mellitus;
D O I
10.1196/annals.1363.019
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mammalian cells are continuously subject to insult from reactive species. Most of the pathogenic mechanisms that have been considered to date reflect overproduction of reactive oxygen species (ROS) or a peculiar failure in intracellular defenses against ROS. We have attempted to consider briefly the most important mechanisms of ROS production, defense, and reactive species-induced cell damage and approaches to therapy, focusing on the example of diabetes mellitus. An improved understanding of these mechanisms should facilitate development of antioxidant intervention strategies leading to reduction in diseases associated with oxidative stress.
引用
收藏
页码:136 / 151
页数:16
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共 61 条
  • [21] N-acetylcysteine and taurine prevent hyperglycemia-induced insulin resistance in vivo: possible role of oxidative stress
    Haber, CA
    Lam, TKT
    Yu, ZW
    Gupta, N
    Goh, T
    Bogdanovic, E
    Giacca, A
    Fantus, IG
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2003, 285 (04): : E744 - E753
  • [22] UCP-mediated energy depletion in skeletal muscle increases glucose transport despite lipid accumulation and mitochondrial dysfunction
    Han, DH
    Nolte, LA
    Ju, JS
    Coleman, T
    Holloszy, JO
    Semenkovich, CF
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2004, 286 (03): : E347 - E353
  • [23] Insulin resistance: From predisposing factor to therapeutic target in type 2 diabetes
    Henry, RR
    [J]. CLINICAL THERAPEUTICS, 2003, 25 : B47 - B63
  • [24] Troglitazone prevents mitochondrial alterations, β cell destruction, and diabetes in obese prediabetic rats
    Higa, M
    Zhou, YT
    Ravazzola, M
    Baetens, D
    Orci, L
    Unger, RH
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1999, 96 (20) : 11513 - 11518
  • [25] Pioglitazone improves insulin secretory capacity and prevents the loss of β-cell mass in obese diabetic db/db mice:: Possible protection of β cells from oxidative stress
    Ishida, H
    Takizawa, M
    Ozawa, S
    Nakamichi, Y
    Yamaguchi, S
    Katsuta, H
    Tanaka, T
    Maruyama, M
    Katahira, H
    Yoshimoto, K
    Itagaki, E
    Nagamatsu, S
    [J]. METABOLISM-CLINICAL AND EXPERIMENTAL, 2004, 53 (04): : 488 - 494
  • [26] The signal transduction function for oxidative phosphorylation is at least second order in ADP
    Jeneson, JAL
    Wiseman, RW
    Westerhoff, HV
    Kushmerick, MJ
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (45) : 27995 - 27998
  • [27] Oxidative stress and the use of antioxidants in diabetes: Linking basic science to clinical practice
    Johansen, Jeanette Schultz
    Harris, Alex K.
    Rychly, David J.
    Ergul, Adviye
    [J]. CARDIOVASCULAR DIABETOLOGY, 2005, 4 (1)
  • [28] The relative contributions of insulin resistance and beta-cell dysfunction to the pathophysiology of Type 2 diabetes
    Kahn, SE
    [J]. DIABETOLOGIA, 2003, 46 (01) : 3 - 19
  • [29] Role of oxidative stress in pancreatic β-cell dysfunction
    Kajimoto, Y
    Kaneto, H
    [J]. MITOCHONDRIAL PATHOGENESIS: FROM GENES AND APOPTOSIS TO AGING AND DISEASE, 2004, 1011 : 168 - 176
  • [30] High protonic potential actuates a mechanism of production of reactive oxygen species in mitochondria
    Korshunov, SS
    Skulachev, VP
    Starkov, AA
    [J]. FEBS LETTERS, 1997, 416 (01) : 15 - 18