Salt Intake, Oxidative Stress, and Renal Expression of NADPH Oxidase and Superoxide Dismutase

Abstract

Abstract. 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 2␣ and malonyldialdehyde were measured in groups (n ϭ 6 to 8) of conscious rats during low-salt, normal-salt, or HS diets. NADPH-and NADH-stimulated superoxide anion (O 2 ·Ϫ ) generation was assessed by chemiluminescence, and expression of NAD(P)H oxidase and SOD were assessed with real-time PCR. Excretion of 8-isoprostane and malonyldialdehyde increased incrementally twoto threefold with salt intake (P Ͻ 0.001), whereas prostaglandin E 2 was unchanged. Renal cortical NADH-and NADPHstimulable O 2 ·Ϫ generation increased (P Ͻ 0.05) 30 to 40% with salt intake. Compared with low-salt diet, HS significantly (P Ͻ 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 ·Ϫ accompanied by enhanced renal expression and activity of NAD(P)H oxidase with diminished renal expression of IC-and Mn-SOD.

The effect of short-term canola oil ingestion on oxidative stress in the vasculature of stroke-prone spontaneously hypertensive rats

“…The decrease in the SOD isoforms indicates a reduced ability to eliminate ·O 2 ˉ in the presence of canola oil and salt. High salt intake (6%) has been shown to reduce renal expression of CuZn-SOD and Mn-SOD in Sprague-Dawley rats [23]. The present study has also showed that p22 phox and NOX2 mRNA expression was reduced in the canola oil group with the presence of salt, indicating that ·O 2 ˉ generated from NADPH oxidase may be decreased.…”

“…The increased plasma and RBC MDA concentration indicates an increased amount of ROS induced lipid peroxidation, which may be due to the salt loading in combination with the diets. A previous study found an increase in urine MDA concentration in Sprague-Dawley rats as a result of salt intake [23]. They found a difference between the low salt (0.03%) and normal salt (0.3) groups, and between the low salt and high salt (6%) groups.…”

“…Evidence has shown that ·O 2 ˉ generated from NAPDP oxidase is increased in hypertension [16]. In addition, Kitiyakara et al found that salt intake in Sprague-Dawley rats lead to an increase in ·O 2 ˉ production [23]. This was accompanied by an increase in renal activity and mRNA expression of NOX2 and p47 phox , and a decrease in CuZn-SOD and MnSOD mRNA expression [23].…”

“…In addition, Kitiyakara et al found that salt intake in Sprague-Dawley rats lead to an increase in ·O 2 ˉ production [23]. This was accompanied by an increase in renal activity and mRNA expression of NOX2 and p47 phox , and a decrease in CuZn-SOD and MnSOD mRNA expression [23]. However, in the vasculature, there are several other sources of ROS, which include: xanthine oxidase, uncoupled nitric oxide synthase, lipoxygenase and the mitochondrial respiratory chain [26,27].…”

“…A recent study showed that dietary phytosterols and phytostanols increase blood pressure in Wistar Kyoto rats in the absence of NaCl loading [21]. Furthermore, research has shown that salt intake can induce oxidative stress, and leads to an increase in ·O 2 ˉ production in SHR and Sprague-Dawley rats [22,23]. More research is required to investigate the effect of canola oil intake on oxidative damage and to examine the changes in the absence of excess dietary salt.…”