Mercuric chloride alters the membrane potential and intracellular calcium level in mouse pancreatic islet cells

J Toxicol Environ Health A. 2002 Feb;65(3-4):317-26. doi: 10.1080/15287390252800891.


In this study, mercuric chloride was applied to the primary cultures of mouse pancreatic islet cells for studying its effects on resting membrane potential and the intracellular free calcium ion concentration ([Ca 2+), using the techniques of electrophysiology and fluorometry. It was observed that mercuric chloride (1-100 microM) caused a rapid and sustained depolarization, and induced a rapid first phase and a large sustained second phase of elevation in fura-2 fluorescence ratio in islet cells. The depolarization and increased lCa2+]i induced by mercuric chloride could be inhibited by dithiothreitol (a sulfhydryl-containing reducing agent). Removing Ca2+ from the external medium inhibited the mercuric chloride-induced elevation of [Ca2+]i. The increased [Ca2+]i may also originate from the endoplasmic reticulum of pancreatic islet cells, since caffeine (an activator of Ca2+ release from endoplasmic reticulum) and thapsigargin (an inhibitor of endoplasmic reticulum Ca2+-ATPase) could antagonize the effect of mercuric chloride. Moreover, in the absence of glucose in the medium, the response of islet cells to mercuric chloride was a rapid first phase of increased [Ca2+]i followed by a small sustained second phase. Readministration of 5 mM glucose was sufficient but transient to restore sustained phase of increased [Ca2+]i. The increase of [Ca2+]i in islet cells induced by a lower concentration of mercuric chloride (5 microM) was potentiated in higher glucose (7.5 mM) medium. Tolbutamide, an inhibitor of the ATP-sensitive K+-channel, could also inhibit the effect of mercuric chloride. These findings suggest that mercuric chloride initially interacts with the sulfhydryl groups of membrane-bound proteins, which may be an ATP-sensitive K+ channel, to cause depolarization of the islet cells. This depolarization triggers Ca2+ influx and then the release of Ca2+ from the endoplasmic reticulum.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / pharmacokinetics*
  • Cell Culture Techniques
  • Disinfectants / adverse effects*
  • Electrophysiology
  • Fluorometry
  • Intracellular Fluid / chemistry
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / physiology*
  • Membrane Potentials / drug effects*
  • Mercuric Chloride / adverse effects*
  • Mice
  • Mice, Inbred ICR


  • Disinfectants
  • Mercuric Chloride
  • Calcium