| Project/Area Number |
03454438
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Functional basic dentistry
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| Research Institution | Kanagawa Dental College |
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Principal Investigator |
OKABE Eiichiro Kanagawa Dental College, Pharmacology, Associate Professor, 歯学部, 助教授 (50097276)
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| Co-Investigator(Kenkyū-buntansha) |
LEE Masaichi Kanagawa Dental College, Pharmacology, Instructor, 歯学部, 助手 (60220795)
TAKAHASHI Shun-suke Kanagawa Dental College, Pharmacology, Instructor, 歯学部, 助手 (60206810)
TOKOKI Kazuo Kanagawa Dental College, Pharmacology, Assistant Professor, 歯学部, 講師 (90139577)
ITO Haruo Kanagawa Dental College, Pharmacology, Professor, 歯学部, 教授 (10084716)
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| Project Period (FY) |
1991 – 1993
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| Keywords | Masseter muscle / Free radicals / Excitation-contraction coupling / Sarcoplasmic reticulum / Calmodulin / Calcium / Ca^<2+> release channel |
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| Research Abstract |
In this research project, we wished to investigate 1) Ca^<2+> kinetics, to characterize 2) the route of Ca^<2+> permeability, to define 3) the role of calmodulin in Ca^<2+> fluxes behavior, and to detrmine 4) the effect of acidosis on the excitation-contraction coupling system and 5) the effect of free oxygen radicals using isolated sarcoplasmic reticulum (SR), myofibrils, or the unfractionated homogenate of canine masseter muscle.
1. The SR from masseter muscle has greater capability of Ca^<2+> release than that from femoral muscle or heart muscle. The passive Ca^<2+> efflux is not carrier mediated, and is not a likely route of Ca^<2+> release during excitation-contraction coupling.
2. Some minimal Ca^<2+> gradient may be required in order to observe a substantial passive Ca^<2+> efflux. It is postulated in this series of research that passive route of efflux during Ca^<2+> accumulation in the SR vesicles is relatively small.
3. Calmodulin-dependent process plays a functional role in the coupling of ATP hydrolysis and Ca^<2+> accumulation through regulation of Ca^<2+> release channels in the SR membrane.
4. Acidosis significantly uncouples Ca^<2+> transport from ATP hydrolysis in the SR and significantly alters myofibrillar ATPase activity. It is hypothesized that these defects may explain an observed depression in skeletal muscle cell function during ischemia.
5. Damage to the masseter muscle is caused by a free radical superoxide anion generated as a result of increased prostaglandins synthesis, and by the production of more lethal hydroxyl radical switched from the production of superoxide anion at low pH.Acidosis can depress SR Ca^<2+> transport in the homogenate of masseter muscle by an oxygen free radical mechanism.
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