Role of Cadmium-Induced Lipid Peroxidation in the Kidney Response to Atrial Natriuretic Hormone

Abstract

In order to investigate the role of increased lipid peroxidation in the development of cadmium-induced hypertension, 30 male albino rats were exposed to drinking water containing 15 µg/ml cadmium for 30 days, and the results were compared with those of 30 controls. Water containing high cadmium concentrations caused a significant accumulation of the element in blood and kidneys, associated with an obvious elevation in blood pressure. The systolic and diastolic blood pressures rose from 102.8 ± 7.0 and 81.2 ± 3.8 mm Hg to 128.1 ± 4.6 and 107.9 ± 7.4 mm Hg, respectively, in cadmium-treated rats (p < 0.01). A decreased glomerular filtration rate and increased serum creati-nine levels were accompanied by elevated levels of cortical and medullary thiobarbituric acid reactive substances in cadmium-induced hypertensive rats. The mean thiobarbituric acid reactive substance level rose from a control value of 211.5 ± 64.1 to 303.3 ± 46.3 nmol/g protein (p < 0.01) in the renal cortex due to the high intake of cadmium. Despite its obvious diuretic and natriuretic action in control animals, the bolus injection of 1.2 and 2.4 µg/kg atrial natriuretic peptide corrected neither elevated blood pressure nor the reduced glomerular filtration rate in rats exposed to cadmium. However, the tubular response to atrial natriuretic peptide remained unaltered. These data suggest that a lack of vascular response to atrial natriuretic peptide is one of the many putative causes of cadmium-induced hypertension, and cadmium-mediated increased lipid peroxidation may be involved in this unresponsiveness.

The Effects of Chronic Cadmium Toxicity on the Hemostatic System

“…Throughout the world, the mean daily cadmium intake of people is 2-6 mg (by oral route, namely intestinal absorption) [26] . The fact that the cadmium doses used in our study and their route of administration are representative of the possible exposure of people to cadmium in their daily lives is significant [15] . Higher blood concentrations of cadmium in the experiment group demonstrate that cadmium toxicity has developed in rats (p !…”

“…Both groups were left to free feeding under equal conditions of care and environment. The control group was fed with normal food and tap water while the cadmium group was fed with food and water containing 15 ppm CdCl 2 in order to create cadmium toxicity at the doses corresponding to those causing chronic cadmium toxicity in human beings [15,26] . After the experimental period of 4 weeks, the rats underwent ketamine anesthesia and their blood was drawn; afterwards the rats were sacrificed.…”

“…It has been demonstrated in many studies that low-dose cadmium causes hypertension in rats [9][10][11][12][13][14][15] .…”

The Effect of Chronic Cadmium Toxicity on Blood Pressure and Plasma Viscosity

“…CdCl 2 (anhydrous) was obtained from Sigma (St. Louis, Mo., USA). The Cd doses used in our investigation and the routes of administration reflect chronic Cd toxicity in daily life [6] .…”

“…Heparinized whole blood samples were dissolved with the microwave digestion method, and samples ready to be measured were kept at 4 ° C [18] . The Cd concentration of blood samples was measured by atomic absorption spectrophotometer, using the graphite furnace method (Z-9000 Graphite furnace apparatus) [6,19] .…”