Zinc-Excess Intake Causes the Deterioration of Renal Function Accompanied by an Elevation in Systemic Blood Pressure Primarily Through Superoxide Radical-Induced Oxidative Stress.

Using rats fed 22 g/d of a control diet containing 0.005% zinc (Zn) or 2 Zn-excess diets containing 0.05% or 0.

Lipopolysaccharide-induced overproduction of nitric oxide and overexpression of iNOS and interleukin-1β proteins in zinc-deficient rats.

Zinc deficiency leads to decreased cellular immune responses. The overproduction of nitrogen species derived from inducible nitric oxide synthase (iNOS), its enzyme, and interleukine-1 beta (IL-1β), and inflammatory cytokine have been implicated in immune responses. The goal of this study was to investigate the effects of lipopolysaccharide (LPS)-induced changes in NO metabolites, iNOS, and IL-1β protein expression in the lungs of zinc-deficient rats.

Ascorbate inhibits apoptosis of Kupffer cells during warm ischemia/reperfusion injury.

Background/aims: This study sought to determine whether ascorbate (Asc), a scavenger of reactive oxygen species, inhibits apoptosis of hepatic cells consisting of hepatocytes, Kupffer cells, and sinusoidal endothelial cells (SECs) in the rat liver after warm ischemia/reperfusion (I/R) injury.

Methodology: Hepatic warm ischemia (69% of the total liver) was induced for 30 min, followed by reperfusion for 60 min. In some animals, ascorbate (at 1 or 10 mg/kg) was infused intravenously immediately before the onset of reperfusion.

Excessive zinc intake elevates systemic blood pressure levels in normotensive rats--potential role of superoxide-induced oxidative stress.

Objectives: The present study was designed to examine whether or not excessive Zn intake affects systemic blood pressure (BP) levels in a normotensive state.

Methods: Systolic BP (SBP) and mean arterial pressure (MAP) before and after administration of the nitric oxide synthase (NOS) inhibitor, N-nitro-L-arginine methyl ester (L-NAME) or the exogenous superoxide scavenger, tempol and the activity of the endogenous superoxide scavenger, Cu/Zn-superoxide dismutase (SOD) and levels of endothelial type (e)NOS mRNA and protein in the thoracic aorta were analyzed in male Sprague-Dawley rats fed a standard diet containing 0.005% Zn or a high Zn diet containing 0.

Detection of prepro-ET-1 mRNA in normal rat kidney by in situ RT-PCR.

Background: Available evidence has shown that endothelin-1 (ET-1) acts in an autocrine/paracrine fashion rather than as a hormone or cytokine. Therefore, the analysis of local ET-1 production is a crucial step toward understanding its physiological and pathophysiological importance. In this study, in situ RT-PCR was utilized to detect tubular expression of prepro-ET-1 mRNA in normal rat kidney.

Decreased expression of brain nitric oxide synthase in macula densa cells and glomerular epithelial cells of rats with mercury chloride-induced acute renal failure.

To elucidate the mechanisms responsible for the development of HgCl(2)-induced acute renal failure (ARF), we examined the expression of brain type (b) nitric oxide synthase (NOS), which is involved in the generation of the vasodilator nitric oxide (NO), in the renal cortex of rats at 20 h after exposure to 7.5 mg/kg HgCl(2). Both blood urea nitrogen and serum creatinine were significantly increased in rats exposed to HgCl(2) relative to control rats, indicating the induction of ARF resulting from HgCl(2) exposure.