Lead (Pb2+) and cadmium (Cd2+) inhibit the dipsogenic action of central beta-adrenergic stimulation by isoproterenol

Abstract

We have previously demonstrated that acute third ventricle injections of both Pb 2+ and Cd 2+ impair the dipsogenic response elicited by three different situations: dehydration and central cholinergic or angiotensinergic stimulation. ß-Adrenergic activation is part of the multifactorial integrated systems operating in drinking behavior control in the central nervous system. In the present study acute third ventricle injections of Pb 2+ (3, 30 and 300 pmol/rat) or Cd 2+ (0.3, 3 and 30 pmol/ rat) blocked the dipsogenic response induced by third ventricle injections of isoproterenol (ISO; 160 nmol/rat) in a dose-dependent manner. Normohydrated animals receiving ISO + NaAc (sodium acetate) or saline (controls) displayed a high water intake after 120 min (ISO + saline = 5.78 ± 0.54 ml/100 g; ISO + NaAc = 6.00 ± 0.6 ml/100 g). After the same period, animals receiving ISO but pretreated with PbAc at the highest dose employed (300 pmol/rat) drank 0.78 ± 0.23 ml/100 g while those receiving ISO and pretreated with the highest dose of CdCl 2 (30 pmol/rat) presented a water intake of 0.7 ± 0.30 ml/100 g. Third ventricle injections of CdCl 2 (3 nmol/rat) or PbAc (3 nmol/rat) did not modify food intake in rats deprived of food for 24 h. Thus, general central nervous system depression explaining the antidipsogenic action of the metals can be safely excluded. It is concluded that both Pb 2+ and Cd 2+ inhibit water intake induced by central ß-adrenergic stimulation. Received April 11, 1996 Accepted December 17, 1996 Key wordsHuman exposure to heavy metals such as cadmium (Cd 2+ ) and lead (Pb 2+ ) may bring about several adverse reactions. Neurotoxicity induced by heavy metals is well-documented in humans and experimental animals (1). Both Cd 2+ and Pb 2+ reach the central nervous system either by crossing the bloodbrain barrier or via retrograde axonal transport (2,3).The presence of heavy metals in the central nervous system disrupts the functional integrity of several neurotransmitter pathways. Many independent reports confirm alterations in brain monoaminergic receptors and uptake after Pb 2+ (4) and Cd 2+ (5,6) intoxication.We have recently used a new approach to study the acute actions of heavy metals on

Central lead administration inhibits water intake and sodium appetite in rats

“…We have demonstrated that acute third ventricle injections of lead in minute amounts induce a significant antidipsogenic effect on dehydrated rats, as well as in those whose drinking was induced by central angiotensinergic, cholinergic and ß-adrenergic stimulation (6,7). This thirst-inhibiting effect of central lead administration may be, at least in part, opioid-dependent, as we have also shown (8).…”

“…We have previously shown that lead injections into the third ventricle induce a significant antidipsogenic ef- fect in several physiological and pharmacological situations (6,7), an effect due, at least partially, to a stimulation of central opioid pathways (8). More recently, we have demonstrated that acute intracerebroventricular injections of lead induce a powerful natriuretic and kaliuretic effect (9).…”

Opiatergic participation in the thirst-inhibiting effect of acute third ventricle injections of cadmium (Cd2+) and lead (Pb2+)

“…Evidently, both things may concomitantly occur. We have previously shown that both cadmium and lead disrupt the thirstgenerating drive exerted by brain angiotensin II as well as by muscarinic and ß-adrenergic activation (7)(8)(9). We have also demonstrated that the antidipsogenic effect of cadmium could be due to 5-HT 2 serotonin receptors activation (8).…”

“…We have demonstrated that both cadmium and lead induce a significant antidipsogenic effect in rats whose water intake was stimulated by dehydration or by third ventricle injections of dipsogenic agents such as angiotensin II, carbachol and isoproterenol (7)(8)(9).…”

Prooxidant-antioxidant balance in the organism of bulls (young cattle) after using cadmium load

“…First of all, introduced intravenously or intraperitoneally cadmium damages the liver, and later on the other organs (Hwang and Wang, 2001;Gutij et al, 2004;Massadeh and Al-Safi, 2005). Toxicity of cadmium element is associated with the ability to generate peroxidation reaction of lipid membranes of hepatocytes (Fregoneze et al, 1997;Watjen and Beyersman, 2004;Uetani et al, 2005). In addition, the activity of some enzymes decreases, in particular, glutathione peroxidase, glutathione reductase, glucose-6-phosphatase, that can be a test for early diagnosis of damaged liver tissue (El-Shahat et al, 2009;Hariv and Gutyj, 2016).…”