Effect of central acute administration of cadmium on drinking behavior

Silva, E. de Castro E; Ferreira, Hadla S.; Cunha, Maurício P.; Bulcao, Christian F.; Sarmento, C; Oliveira, IR De; Fregoneze, J.B.

doi:10.1016/0091-3057(95)02070-5

Cited by 23 publications

(3 citation statements)

References 33 publications

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“…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).…”

Section: Time (Min)mentioning

confidence: 89%

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

de-Castro-e-Silva¹,

Luz²,

Sarmento³

et al. 1998

Braz J Med Biol Res

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We have previously demonstrated that acute third ventricle injections of both lead and cadmium prevent the dipsogenic response elicited by dehydration or by central injections of dipsogenic agents such as angiotensin II, carbachol and isoproterenol in rats. We have also shown that the antidipsogenic action of cadmium may be due, at least in part, to activation of thirst-inhibitory central serotonergic pathways. In the present paper we show that in Wistar male rats the antidipsogenic effect of both lead acetate (3.0 nmol/rat) and cadmium chloride (3.0 nmol/rat) may be partially dependent on the activation of brain opiatergic pathways since central injections of naloxone (82.5 nmol/ rat), a non-selective opioid antagonist, blunt the thirst-inhibiting effect of these metals. One hundred and twenty minutes after the second third ventricle injections, dehydrated animals (14 h overnight) receiving saline + sodium acetate displayed a high water intake (7.90 ± 0.47 ml/100 g body weight) whereas animals receiving saline + lead acetate drank 3.24 ± 0.47 ml/100 g body weight. Animals receiving naloxone + lead acetate drank 6.94 ± 0.60 ml/100 g body weight. Animals receiving saline + saline drank 8.16 ± 0.66 ml/100 g body weight whilst animals receiving saline + cadmium chloride drank 1.63 ± 0.37 ml/100 g body weight. Animals receiving naloxone + cadmium chloride drank 8.01 ± 0.94 ml/100 g body weight. It is suggested that acute third ventricle injections of both lead and cadmium exert their antidipsogenic effect by activating thirst-inhibiting opioid pathways in the brain. Correspondence

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Section: Time (Min)mentioning

confidence: 89%

“…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).…”

mentioning

confidence: 99%

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

de-Castro-e-Silva¹,

Luz²,

Sarmento³

et al. 1998

Braz J Med Biol Res

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“…We have recently reported that acute injections of PbAc (7) or CdCl 2 (8) into the third ventricle of rats block the dipsogenic response induced by three different situations, i.e., water deprivation and central cholinergic or angiotensinergic stimulation. The data now included in the present paper clearly show that both Cd 2+ and Pb 2+ are also capable of decreasing water intake following central ß-adrenergic stimulation.…”

Section: Timementioning

confidence: 99%

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

Fregoneze

Marinho²,

Soares³

et al. 1997

Braz J Med Biol Res

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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

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Acute enhancement of non‐rapid eye movement sleep in rats after drinking water contaminated with cadmium chloride

Unno

Yamoto

Takeuchi

et al. 2013

J of Applied Toxicology

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Cadmium (Cd) is a heavy metal widely used or effused by industries. Serious environmental Cd pollution has been reported over the past two centuries, whereas the mechanisms underlying Cd-mediated diseases are not fully understood. Interestingly, an increase in reactive oxygen species (ROS) after Cd exposure has been shown. Our group has demonstrated that sleep is triggered via accumulation of ROS during neuronal activities, and we thus hypothesize the involvement of Cd poisoning in sleep-wake irregularities. In the present study, we analyzed the effects of Cd intake (1-100 ppm CdCl₂ in drinking water) on rats by monitoring sleep encephalograms and locomotor activities. The results demonstrated that 100 ppm CdCl₂ administration for 28 h was sufficient to increase non-rapid-eye-movement (non-REM) sleep and reduce locomotor activities during the night (the rat active phase). In contrast, free-running locomotor rhythms under constant dim red light and their re-entrainment to 12:12-h light/dark cycles were intact under chronic (1 month) 100 ppm CdCl₂ administrations, suggesting a limited influence on circadian clock movements at this dosage. The relative amount of oxidized glutathione increased in the brain after the 28-h 100 ppm CdCl₂ administrations similar to the levels in cultured astrocytes receiving H₂O₂ or CdCl₂ in culture medium. Therefore, we propose Cd-induced sleep as a consequence of oxidative stress. As oxidized glutathione is an endogenous sleep substance, we suggest that Cd rapidly induces sleepiness and influences activity performance by occupying intrinsic sleep-inducing mechanisms. In conclusion, we propose increased non-REM sleep during the active phase as an index of acute Cd exposure.

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Effect of central acute administration of cadmium on drinking behavior

Cited by 23 publications

References 33 publications

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

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

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

Acute enhancement of non‐rapid eye movement sleep in rats after drinking water contaminated with cadmium chloride

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