Effect of the sulfhydryl reagent thimerosal on cytosolic free Ca2+ and membrane potential of thymocytes

Gukovskaya, Anna S.; Trepakova, Elena S.; Зинченко, В. П.; Korystov, Yuri N.; Безуглов, В. В.

doi:10.1016/0005-2736(92)90275-q

Cited by 17 publications

(7 citation statements)

References 24 publications

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“…It was shown that the SH‐reagent thimerosal induced the rise of [Ca 2+ ] i in T cells by inhibiting PM Ca 2+ ‐ATPases and opening Ca 2+ channels [14]. As shown in Fig.…”

Section: Resultsmentioning

confidence: 86%

A comparative study of the calcium system in memory T cells and naive T cells

et al. 1999

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The comparative analysis of responses of memory and naive T lymphocytes to Ca P+ -mobilizing agents, namely Con A, thimerosal, thapsigargin and ionomycin, was carried out. The effect of these agents on both types of T cells differed qualitatively and quantitatively. The lack of intracellular Ca P+ stores in memory T cells was shown. Ca P+ -mobilizing agents did not induce influx of Ca P+ in memory T cells from outside and this was the reason for their stability to Ca P+ ionophores. It was also shown that memory T cells were resistant to the`Ca P+ paradox'.z 1999 Federation of European Biochemical Societies.

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“…It was shown that the SH‐reagent thimerosal induced the rise of [Ca 2+ ] i in T cells by inhibiting PM Ca 2+ ‐ATPases and opening Ca 2+ channels [14]. As shown in Fig.…”

Section: Resultsmentioning

confidence: 86%

A comparative study of the calcium system in memory T cells and naive T cells

et al. 1999

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“…An in vitro study found that thimerosal blocked ATP dependent potassium channel opening by the opener P1075, 19) while other studies have reported an effect similar to ATP dependent potassium channel blockers, ie, that it increases calcium-loading to the cell. [12][13][14] Pinacidil acts as an opener and has the opposite effect of ATP dependent potassium channel blockers on the action potential duration. 20,31) Pinacidil alone decreased the severity of arrhyth-Vol 46 No 4 mia, like thimerosal.…”

Section: Discussionmentioning

confidence: 99%

“…9,10) In several studies, it was shown that it increases intracellular calcium and leads to calcium loading, like ATP dependent channel blockers. [11][12][13] Thimerosal causes long-lasting relaxation in smooth muscle 14) and has been suggested to produce endothelially-derived coronary dilatation.…”

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confidence: 99%

Effect of Thimerosal on Arrhythmia Induced by Coronary Ligation The Involvement of ATP-dependent Potassium Channels

et al. 2005

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SUMMARYThiol-modifying agents induce the release of nitric oxide (NO) from endothelial epithelium and the release of reactive oxygen free radicals in the vascular system. Moreover, thiol groups are essential for the functioning of the ATP dependent potassium channel (K-ATP). The effects of thiol-modifying agents and their molecular mechanisms on arrhythmia have not been widely studied. In this study, we investigated the effect of the hydrophilic SH-group-oxidizing substance thimerosal on the arrhythmia induced by reperfusion/ischemia after coronary artery ligation in rats. We studied the possible involvement of the K-ATP and NOS on the effect of thimerosal. Thimerosal pretreatment (3, 30 mg/kg dose iv. 10 minutes before coronary occlusion) significantly decreased the length of total arrhythmia, ventricular tachycardia, and the arrhythmia score. This effect of thimerosal was reversed by the K-ATP opener pinacidil but not by the K-ATP blocker glibenclamide. The inhibition of iNOS by L-NAME did not alter the antiarrhythmic effect of thimerosal. These data clearly suggest that the antiarrhythmic effect of thimerosal is dependent upon the blockage of K-ATP. ( 1) The activity of some K + channels is drastically altered by the oxidation of critical SH-groups of the channel protein. An interesting example is the loss of rapid inactivation of the voltage-gated K + channel RCK4 (Kv1.4) produced by oxidation of a thiol group; this residue is located near the intracellular inactivation (ball) domain of the channel.2) ATP-sensitive K + channels (K-ATP channels) in skeletal muscle, 3,4) heart 5) and pancreatic β-cells or insulin-secreting cellFrom the

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“…The -SH group of oxidizing agents has been shown to influence the function of Ca 2 + channels (9,10). The effect of thimerosal, a sulfhydryl oxidizing reagent, on [Ca 2 + ] i homeostasis is complex and varies with dose and cell type.…”

Section: Introductionmentioning

confidence: 99%

“…The effect of thimerosal, a sulfhydryl oxidizing reagent, on [Ca 2 + ] i homeostasis is complex and varies with dose and cell type. It has been reported that thimerosal induced [Ca 2 + ] i mobilization in rat thymocytes (10), human endothelial cells (11) and thymus lymphocytes (12) at concentrations ranging from 5-100 vM. In some cases, it was proposed that thimerosal induces an increase in [Ca 2 + ] i by sensitiz-ing the InsP 3 receptor (13).…”

Section: Introductionmentioning

confidence: 99%

Thimerosal-induced Ca2+ Mobilization in Isolated Guinea Pig Cochlear Outer Hair Cells

Chen

Harada²,

Yamashita³

1998

Acta Oto-Laryngologica

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Chen L, Harada N, Yamashita T. Thimerosal-induced Ca 2 + mobilization in isolated guinea pig cochlear outer hair cells. Acta Otolaryngol (Stockh) 1998; Suppl 539: 28-33.Intracellular calcium mobilization of isolated guinea pig cochlear outer hair cells (OHCs) was investigated using thimerosal, a -SH group oxidizing agent, and fura-2 fluorescence ratio imaging microscopy. In the presence of thimerosal, intracellular Ca 2 + concentrations ([Ca 2 + ] i ) of OHCs were elevated in a dose-dependent manner. Even in Ca 2 + -free medium, Ca 2 + response was still induced. The effects of thimerosal on [Ca 2 + ] i were completely blocked and reversed by dithiothreiotol (DTT). Neither 1-100 vM ryanodine nor 5-20 mM caffeine altered the effects of thimerosal. Pretreatment with pertussis toxin (PTX) for 30 min did not affect the thimerosal-induced increase in [Ca 2 + ] i . The increase in [Ca 2 + ] i when Ca 2 + was added during thimerosal application in Ca 2 + -free medium was almost completely blocked by 500 vM LaCl 3 , while nifedipine did not inhibit further increase in [Ca 2 + ] i caused by thimerosal. Thus, oxidation of the -SH group of the OHC membrane can induce a Ca 2 + release from intracellular Ca 2 + stores, which are ryanodine-and caffeine-insensitive, and Ca 2 + influx through non-specific Ca 2 + channels, but not the nifedipine-sensitive Ca 2 + channels. The possible oxidation of -SH group gated Ca 2 + channels in OHCs is worthy of further study.

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Effect of the sulfhydryl reagent thimerosal on cytosolic free Ca2+ and membrane potential of thymocytes

Cited by 17 publications

References 24 publications

A comparative study of the calcium system in memory T cells and naive T cells

A comparative study of the calcium system in memory T cells and naive T cells

Effect of Thimerosal on Arrhythmia Induced by Coronary Ligation The Involvement of ATP-dependent Potassium Channels

Thimerosal-induced Ca2+ Mobilization in Isolated Guinea Pig Cochlear Outer Hair Cells

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