Salt intake, oxidative stress, and renal expression of NADPH oxidase and superoxide dismutase

被引:266
作者
Kitiyakara, C
Chabrashvili, T
Chen, YF
Blau, J
Karber, A
Aslam, S
Welch, WJ
Wilcox, CS
机构
[1] Georgetown Univ, Div Nephrol & Hypertens, Washington, DC USA
[2] Georgetown Univ, Cardiovasc Kidney Inst, Washington, DC USA
来源
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY | 2003年 / 14卷 / 11期
关键词
D O I
10.1097/01.ASN.0000092145.90389.65
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
The hypothesis that a high salt (HS) intake increases oxidative stress was investigated and was related to renal cortical expression of NAD(P)H oxidase and superoxide dismutase (SOD). 8-Isoprostane PGF(2alpha) and malonyldialdehyde were measured in groups (n = 6 to 8) of conscious rats during low-salt, normal-salt, or HS diets. NADPH- and NADH-stimulated superoxide anion (O-2(-)) generation was assessed by chemiluminescence, and expression of NAD(P)H oxidase and SOD were assessed with real-time PCR. Excretion of 8-iso-prostane and malonyldialdehyde increased incrementally two-to threefold with salt intake (P < 0.001), whereas prostaglandin E-2 was unchanged. Renal cortical NADH- and NADPH- stimulable O-2(-) generation increased (P < 0.05) 30 to 40% with salt intake. Compared with low-salt diet, HS significantly (P < 0.005) increased renal cortical mRNA expression of gp91(phox) and P47(phox) and decreased expression of intracellular CuZn (IC)-SOD and mitochondrial (Mn)-SOD. Despite suppression of the renin-angiotensin system, salt loading enhances oxidative stress. This is accompanied by increased renal cortical NADH and NADPH oxidase activity and increased expression of gp91(phox) and P47(phox) and decreased IC- and Mn-SOD. Thus, salt intake enhances generation of O-2(-) accompanied by enhanced renal expression and activity of NAD(P)H oxidase with diminished renal expression of IC- and Mn-SOD.
引用
收藏
页码:2775 / 2782
页数:8
相关论文
共 48 条
  • [1] NADPH oxidase: An update
    Babior, BM
    [J]. BLOOD, 1999, 93 (05) : 1464 - 1476
  • [2] Barton M, 2000, J AM SOC NEPHROL, V11, P835, DOI 10.1681/ASN.V115835
  • [3] Long-term antioxidant administration attenuates mineralocorticoid hypertension and renal inflammatory response
    Beswick, RA
    Zhang, HF
    Marable, D
    Catravas, JD
    Hill, WD
    Webb, RC
    [J]. HYPERTENSION, 2001, 37 (02) : 781 - 786
  • [4] Glucose-induced oxidative stress in mesangial cells
    Catherwood, MA
    Powell, LA
    Anderson, P
    McMaster, D
    Sharpe, PC
    Trimble, ER
    [J]. KIDNEY INTERNATIONAL, 2002, 61 (02) : 599 - 608
  • [5] Effects of ANG II type 1 and 2 receptors on oxidative stress, renal NADPH oxidase, and SOD expression
    Chabrashvili, T
    Kitiyakara, C
    Blau, J
    Karber, A
    Aslam, S
    Welch, WJ
    Wilcox, CS
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 2003, 285 (01) : R117 - R124
  • [6] Expression and cellular localization of classic NADPH oxidase subunits in the spontaneously hypertensive rat kidney
    Chabrashvili, T
    Tojo, A
    Onozato, ML
    Kitiyakara, C
    Quinn, MT
    Fujita, T
    Welch, WJ
    Wilcox, CS
    [J]. HYPERTENSION, 2002, 39 (02) : 269 - 274
  • [7] Salt intake and renal outcome in patients with progressive renal disease
    Cianciaruso, B
    Bellizzi, V
    Minutolo, R
    Tavera, A
    Capuano, A
    Conte, G
    De Nicola, L
    [J]. MINERAL AND ELECTROLYTE METABOLISM, 1998, 24 (04) : 296 - 301
  • [8] Davis CA, 2001, J AM SOC NEPHROL, V12, P2683, DOI 10.1681/ASN.V12122683
  • [9] Dworkin LD, 1996, J AM SOC NEPHROL, V7, P437
  • [10] p22phox mRNA expression and NADPH oxidase activity are increased in aortas from hypertensive rats
    Fukui, T
    Ishizaka, N
    Rajagopalan, S
    Lauren, JB
    Capers, Q
    Taylor, WR
    Harrison, DG
    deLeon, H
    Wilcox, JN
    Griendling, KK
    [J]. CIRCULATION RESEARCH, 1997, 80 (01) : 45 - 51