Acute and Chronic Effect of Ethanol on (Na + K)-ATPase Activity and Cyclic AMP Response to Vasopressin in Rat Papillary Collecting Duct Cells

Rodrigo, Ramón; Thielemann, Lilian; Orellana, Myriam

doi:10.1016/s0306-3623(97)00380-7

Cited by 15 publications

(8 citation statements)

References 21 publications

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“…[24] The loss of Na + observed in conscious animals infused with methylated spirits alone and in combination with nicotine was in contrast to the renal Na + retention observed in ethanoladministered rats [10] attributable to an increase in Na + /K + ATPase activity in the cortex and outer medulla. [25,26] In the current study, in animals sacrificed at week 4, elevated aldosterone levels were associated with increased plasma concentrations of Na + (see Table 2). This suggests a direct patho-physiological effect of methanol on renal function, [27] possibly at the level of the proximal and distal convoluted tubules to disrupt the ALD-mediated retention of Na + .…”

Section: Discussionmentioning

confidence: 49%

Renal Function in Male Sprague-Dawley Rats Concurrently Exposed to Long-Term Nicotine (3-{1-Methyl-2-Pyrrolidinyl}Pyridine) and Methylated Spirits (Methyl Alcohol)

2008

Renal Failure

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Abuse of nicotine and methylated spirits is a global problem. The current study determined the concurrent influence of nicotine and methylated spirits on renal hemodynamics. Two series of experimental protocols were designed: conscious and anesthetized vehicle loading. Conscious animals received nicotine (0.1 mg.kg -1 bwt, 0.26-0.30 mL), methylated spirits (1.0 g.kg -1 bwt, 0.26-0.30 mL), combined nicotine and methylated spirits, and control animals (water, 0.26-0.30 mL). Anesthetized animals were challenged with a continuous jugular infusion of 0.077M NaCl. Plasma nicotine concentration was significantly elevated in combined conscious treatments by comparison with animals infused nicotine alone. Plasma arginine vasopressin was significantly attenuated in combined conscious groups, and those infused methylated spirits alone. Aldosterone was elevated in all conscious groups. Both plasma ethanol and methanol concentrations were elevated in rats concurrently administered nicotine and methylated spirits compared with those given methylated spirits alone. Urinary Na + levels were significantly elevated in all anesthetized groups associated with attenuated aldosterone concentrations. Plasma nicotine concentrations were increased in combined treatments. Plasma ethanol levels were significantly reduced and elevated in rats concurrently exposed to nicotine and methylated spirits, respectively. The present study suggests that chronic exposure to methylated spirits alone and in combination with nicotine increases urinary Na + loss. The renal toxicity is manifested hypothetically via elevations in plasma nicotine and methanol concentrations. This implies that people who concurrently consume methylated spirits and smoke cigarettes have an increased risk of renal failure by being predisposed to fluid and electrolyte disturbances.

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Section: Discussionmentioning

confidence: 49%

Renal Function in Male Sprague-Dawley Rats Concurrently Exposed to Long-Term Nicotine (3-{1-Methyl-2-Pyrrolidinyl}Pyridine) and Methylated Spirits (Methyl Alcohol)

2008

Renal Failure

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“…Impaired function of histiotrophic nutrition will lead to retarded growth and malformations of the embryo, which has been reported by previous studies (Balkan et al, 1989;Hunter et al, 1991;Ambroso and Harris, 1993). We considered that the reasons for such alterations might be: (i) the free radicals produced by ethanol metabolism might cause lipid peroxidation of the cell membrane (Kotch et al, 1995;Chen and Sulik, 1996); (ii) ethanol might inhibit the activity of the ATPase located in the microvilli side cell membrane and mitochondrial membrane (Rodrigo, et al, 1998;Sepulveda and Mata, 2004), and so effect pinocytosis and storage vesicle transport; and (iii) ethanol might disturb the transmission of pinocytosis related biochemical signals.…”

Section: Discussionmentioning

confidence: 88%

Effect of ethanol on the development of visceral yolk sac

Xiao

2005

Human Reproduction

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BACKGROUND: Prenatal ethanol exposure can cause development retardation and malformations in human offspring. Before the formation of chorioallantoic placenta, yolk sac plays an important role in transporting nutrients from the mother to the embryo. Functional suppression of yolk sac is found to be relevant to the malformations in mammalian embryos. METHODS: Female 8.5-day C57BL/6J mouse embryos were cultured in vitro and exposed to different doses of ethanol. The development of visceral yolk sac (VYS) was examined with light and electron microscopes. The expression profiles of some vasculogenesis-related genes were detected with reverse transcription -PCR. RESULTS: A dose-dependent toxicity to the VYS was found, including reduced diameter, decreased protein and DNA contents, and suppressed development of vitelline vessels. The hypogenesis of VYS agreed with the retarded development and/or malformations found in the embryos. Histological and functional alterations were found in the ethanol-exposed VYS endodermal cells. The expressions of vasculogenesis-related genes, fetal liver kinase 1 (Flk1) and tyrosine kinase with immunoglobulin and epidermal growth factor homology domains 2 (Tie2), were repressed by ethanol. CONCLUSIONS: Impaired structural and functional development of VYS may contribute to the teratogenic action of ethanol in mice, which may also provide a clue to the study of fetal alcohol syndrome in humans.

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“…Acute ethanol administration increases the membrane fluidity [60-62], whereas chronic alcohol intake decreases the fluidity of membranes [60,63,64], which become more tolerant to the disordering effect of ethanol [60,63]. Acute ethanol exposure also decreases Na + /K + -ATPase activity in the cerebral cortex and brain stem [65] and kidneys of adult rats [66]. …”

Section: Discussionmentioning

confidence: 99%

Neuroprotection by taurine in ethanol-induced apoptosis in the developing cerebellum

et al. 2010

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BackgroundAcute ethanol administration leads to massive apoptotic neurodegeneration in the developing central nervous system. We studied whether taurine is neuroprotective in ethanol-induced apoptosis in the mouse cerebellum during the postnatal period.MethodsThe mice were divided into three groups: ethanol-treated, ethanol+taurine-treated and controls. Ethanol (20% solution) was administered subcutaneously at a total dose of 5 g/kg (2.5 g/kg at time 1 h and 2.5 g/kg at 3 h) to the ethanol and ethanol+taurine groups. The ethanol+taurine group also received two injections of taurine (1 g/kg each, at time zero and at 4 h). To estimate apoptosis, immunostaining for activated caspase-3 and TUNEL staining were made in the mid-sagittal sections containing lobules I-X of the cerebellar vermis at 12 or 8 hours after the first taurine injection. Changes in the blood taurine level were monitored at each hour by reverse-phase high-performance liquid chromatography (HPLC).ResultsEthanol administration induced apoptosis of Purkinje cells on P4 in all cerebellar lobules, most extensively in lobules IX and X, and on P7 increased the number of activated caspase-3-immunoreactive and TUNEL-positive cells in the internal layer of the cerebellum. Administration of taurine significantly decreased the number of activated caspase-3-immunoreactive and TUNEL-positive cells in the internal layer of the cerebellum on P7, but had no effect on Purkinje cells in P4 mice. The high initial taurine concentration in blood of the ethanol+taurine group diminished dramatically during the experiment, not being different at 13 h from that in the controls.ConclusionsWe conclude that the neuroprotective action of taurine is not straightforward and seems to be different in different types of neurons and/or requires prolonged maintenance of the high taurine concentration in blood plasma.

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Acute and Chronic Effect of Ethanol on (Na + K)-ATPase Activity and Cyclic AMP Response to Vasopressin in Rat Papillary Collecting Duct Cells

Cited by 15 publications

References 21 publications

Renal Function in Male Sprague-Dawley Rats Concurrently Exposed to Long-Term Nicotine (3-{1-Methyl-2-Pyrrolidinyl}Pyridine) and Methylated Spirits (Methyl Alcohol)

Renal Function in Male Sprague-Dawley Rats Concurrently Exposed to Long-Term Nicotine (3-{1-Methyl-2-Pyrrolidinyl}Pyridine) and Methylated Spirits (Methyl Alcohol)

Effect of ethanol on the development of visceral yolk sac

Neuroprotection by taurine in ethanol-induced apoptosis in the developing cerebellum

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