Low micromolar concentrations of cadmium and mercury ions activate peritubular membrane K+ conductance in proximal tubular cells of frog kidney

Toxic metals such as cadmium (Cd(2+)) pose serious risks to human health. However, even though the importance of Cd(2+) as environmental health hazards is now widely appreciated, the specific mechanisms by which it produces its adverse effects have yet to be fully elucidated. Cd(2+) is known to enter cells, it binds and interacts with a multitude of molecules, it may indirectly induce oxidative stress and interfere with gene expression and repair of DNA. It also interacts with transport across cell membranes and epithelia and may therefore disturb the cell's homeostasis and function. Interaction with epithelial transport, especially in the kidney and the liver, may have serious consequences in general health. A lot of research still needs to be done to understand the exact way in which Cd(2+) interferes with these transport phenomena. It is not always clear whether Cd(2+) has primary or secondary effects on cell membrane transport. In the present review we try to summarize the work that has been done up to now and to critically discuss the relevance of the experimental work in vitro with respect to the in vivo situation.

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“…caused a comparable increase in K ? conductance when applied from the basolateral side(Nesovic-Ostojic et al 2008).…”

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confidence: 99%

Cadmium and transport of ions and substances across cell membranes and epithelia

2010

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“…Wiggers et al used lower doses of mercury and showed a reduction in the participation of potassium channels in mesenteric resistance arteries. However, other authors have demonstrated that acute incubation with different concentrations of mercury can stimulate or suppress potassium efflux currents that are sensitive to TEA or glibenclamide in human B lymphocytes, proximal tubular cells of the frog kidney and rat thoracic aorta . Because endothelial NO can directly activate the potassium channels, especially BK Ca , and ROS can negatively modulate the activity of these channels, we evaluated the vasodilatation in response to the NO donor SNP after a pre‐incubation with tiron to test the response to a known amount NO without the influence of local ROS.…”

Section: Discussionmentioning

confidence: 99%

Impaired participation of potassium channels and Na⁺/K⁺‐ATPase in vasodilatation due to reduced nitric oxide bioavailability in rats exposed to mercury

Botelho

Marques

Lima

et al. 2018

Basic Clin Pharma Tox

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Mercury intoxication is a public health risk factor due to its hazardous effect to several organs, including the cardiovascular system. There is evidence of endothelial dysfunction after exposure to mercury, but the effects on endothelium-dependent vasodilatation are still unknown. In the present study, we aimed to evaluate the chronic effects of high HgCl doses on the mechanisms of vasodilatation. Wistar rats were injected with HgCl (1st dose 10.86 μg/kg, and daily doses 0.014 μg/kg for 30 days i.m.), and saline was used as control. Mercury exposure reduced the acetylcholine-induced vasodilatation in aortic rings, which was restored by incubation with antioxidant tiron. Inhibition of the NO synthase, Na /K -ATPase and K channels indicates reduced participation of these factors. In the mercury group, there were an increased local anion superoxide and a reduced NO. The vasodilatation to exogenous NO was partially inhibited by co-incubation with TEA plus tiron, suggesting that reduced NO bioavailability is the responsible to that decreased the participation of K channels. Moreover, there was an increased participation of the Na /K -ATPase associated with an up-regulation of its alpha-1 subunit. In conclusion, reduced NO bioavailability plays a major role in the impaired participation of K channels and Na /K -ATPase in the acetylcholine-mediated relaxation, although sodium pump is up-regulated probably as a compensatory mechanism.

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p38 MAPK as a signal transduction component of heavy metals stress in Euglena gracilis

et al. 2008

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Living organisms are subject to stress, and among these stressors, heavy metals exposure triggers accumulation of sulfur metabolites. Among these metabolites, glutathione and phytochelatins are found in several organisms, such as Euglena gracilis. Pre-exposing E. gracilis to low concentrations of Hg2+ generates a population with resistance to even 0.2 mM Cd2+, and this resistance relies partly on phytochelatins. p38 MAPK is stimulated by stress and is involved in apoptotic as well as survival mechanisms. In this study, we explored its participation in heavy metal-induced stress and its possible role in sulfur metabolite accumulation. We found that about 51% of the E. gracilis pretreated with Hg2+ becomes resistant to Cd2+ and proliferates despite the presence of this metal. The accumulation of the sulfur metabolites gamma-glu-cys, glutathione and phytochelatin 2 displayed cyclic patterns that were disturbed by a challenge with Cd2+. We observed a p38 MAPK-like activity that was stimulated by acute or chronic heavy metal exposure, and its inhibition by SB203580 slightly diminished the accumulation of sulfur compounds. p38 MAPK inhibition also affected basal levels of glutathione in either pretreated or control cells. Thus, it appears that p38 MAPK mediates redox stress component of the signal pathway induced by heavy metals.

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Low micromolar concentrations of cadmium and mercury ions activate peritubular membrane K+ conductance in proximal tubular cells of frog kidney

Cited by 7 publications

References 38 publications

Cadmium and transport of ions and substances across cell membranes and epithelia

Cadmium and transport of ions and substances across cell membranes and epithelia

Impaired participation of potassium channels and Na⁺/K⁺‐ATPase in vasodilatation due to reduced nitric oxide bioavailability in rats exposed to mercury

p38 MAPK as a signal transduction component of heavy metals stress in Euglena gracilis

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Low micromolar concentrations of cadmium and mercury ions activate peritubular membrane K+ conductance in proximal tubular cells of frog kidney

Cited by 7 publications

References 38 publications

Cadmium and transport of ions and substances across cell membranes and epithelia

Cadmium and transport of ions and substances across cell membranes and epithelia

Impaired participation of potassium channels and Na+/K+‐ATPase in vasodilatation due to reduced nitric oxide bioavailability in rats exposed to mercury

p38 MAPK as a signal transduction component of heavy metals stress in Euglena gracilis

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Impaired participation of potassium channels and Na⁺/K⁺‐ATPase in vasodilatation due to reduced nitric oxide bioavailability in rats exposed to mercury