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Related Experiment Videos

Critical sulfhydryls regulate calcium release from sarcoplasmic reticulum.

J J Abramson1, G Salama

  • 1Physics Department, Portland State University, Oregon 97207.

Journal of Bioenergetics and Biomembranes
|April 1, 1989
PubMed
Summary

Heavy metals and other compounds trigger rapid calcium (Ca2+) release from the sarcoplasmic reticulum (SR) by oxidizing sulfhydryl (SH) groups. This oxidation opens the SR Ca2+ release channel, influencing muscle contraction.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Muscle Physiology

Background:

  • The sarcoplasmic reticulum (SR) is crucial for regulating intracellular calcium (Ca2+) levels in muscle cells.
  • Rapid Ca2+ release from the SR initiates muscle contraction.
  • The role of sulfhydryl (SH) groups in Ca2+ release channels is not fully understood.

Purpose of the Study:

  • To investigate the mechanisms by which heavy metals and other compounds trigger Ca2+ release from the SR.
  • To elucidate the role of sulfhydryl (SH) group oxidation in regulating the SR Ca2+ release channel.
  • To propose a model for Ca2+ channel gating based on SH group redox state.

Main Methods:

  • Monitoring Ca2+ release using isolated SR vesicle preparations.
  • Assessing Ca2+ release indirectly via phasic contractions in skinned muscle fibers.

Related Experiment Videos

  • Utilizing agents like Cu2+/mercaptans, phthalocyanine dyes, reactive disulfides, and anthraquinones to induce SH oxidation.

    • Main Results:

    • Ca2+ release from the SR can be rapidly triggered by agents that oxidize sulfhydryl (SH) groups to disulfides.
    • These triggering agents appear to directly interact with the Ca2+ release protein in the SR.
    • Oxidation and reduction of endogenous SH groups were shown to reversibly control the opening and closing of the SR Ca2+ release channel.

    Conclusions:

    • Sulfhydryl (SH) group oxidation is a key mechanism for regulating Ca2+ release from the sarcoplasmic reticulum.
    • The Ca2+ release channel can be modulated by reversible redox changes in its SH groups.
    • This finding provides a model for understanding how external stimuli can influence muscle excitation-contraction coupling.