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G Saito

Publications and source records attributed to G Saito.

At least 55 records · Page 3Linked to original sources
PubMed1989

[Steady-state calcium accumulation and its reduction by caffeine in sarcoplasmic reticulum from masseter muscle].

The passive Ca2+ efflux pathways in skeletal sarcoplasmic reticulum (SR) vesicles include the efflux through a Ca2+ channel and a passive leak parallel to the channel and the pump. It is known that caffeine stimulates Ca(2+)-induced Ca2+ release. To gain further insight into the effect of caffeine on Ca2+ flux behavior of canine masseter muscle SR vesicles, the present study focuses on the interaction of steady-state Ca2+ accumulation and passive Ca2+ permeability in the presence or absence of endogenous calmodulin (CaM), which is known to regulate Ca2+ release channel. Caffeine (1) produced ruthenium red- or endogenous CaM-inhibitable reduction of oxalate-supported Ca2+ uptake velocity with no effect on Ca2+, Mg(2+)-ATPase activity; (2) reduced steady-state Ca2+ uptake; and (3) had no effect on the permeability of the SR vesicles to Ca2+, determined by measuring net efflux of Ca2+ after stopping pump mediated fluxes, suggesting that passive Ca2+ permeability is unimportant pathway for changing steady-state Ca2+ accumulation. The inhibitory effect of caffeine on steady-state Ca2+ uptake was moderately abolished by the removal of endogenous CaM from SR vesicles. Inositol 1,4,5-trisphosphate (IP3) caused the same effect as that of caffeine on oxalate-supported Ca2+ uptake velocity, steady-state Ca2+ uptake and passive Ca2+ permeability. In summary, the data reveal that caffeine (1) inhibits oxalate entry pathway via inhibition of CaM, and (2) directly modifies CaM-dependent component of Ca2+ fluxes in the SR and reduces steady-state Ca2+ accumulation due to increased Ca2+ release through a Ca2+ efflux pathway which is inhibited by CaM but not due to reduced catalytic activity of the pump; and that the masseter muscle SR vesicles include IP3-sensitive Ca2+ release channel.

Animals↗
PubMed1987

Calmodulin participation in oxygen radical-induced cardiac sarcoplasmic reticulum calcium uptake reduction.

The effect of scavengers of oxygen radicals on canine cardiac sarcoplasmic reticulum (SR) Ca2+ uptake velocity was investigated at pH 6.4, the intracellular pH of the ischemic myocardium. With the generation of oxygen radicals from a xanthine-xanthine oxidase reaction, there was a significant depression of SR Ca2+ uptake velocity. Xanthine alone or xanthine plus denatured xanthine oxidase had no effect on this system. Superoxide dismutase (SOD), a scavenger of .O2-, or denatured SOD had no effect on the depression of Ca2+ uptake velocity induced by the xanthine-xanthine oxidase reaction. However, catalase, which can impair hydroxyl radical (.OH) formation by destroying the precursor H2O2, significantly inhibited the effect of the xanthine-xanthine oxidase reaction. This effect of catalase was enhanced by SOD, but not by denatured SOD. Dimethyl sulfoxide (Me2SO), a known .OH scavenger, completely inhibited the effect of the xanthine-xanthine oxidase reaction. The observed effect of oxygen radicals and radical scavengers was not seen in the calmodulin-depleted SR vesicles. Addition of exogenous calmodulin, however, reproduced the effect of oxygen radicals and the scavengers. The effect of oxygen radicals was enhanced by the calmodulin antagonists (compounds 48/80 and W-7) at concentrations which showed no effect alone on Ca2+ uptake velocity. Taken together, these findings strongly suggest that .OH, but not .O2-, is involved in a mechanism that may cause SR dysfunction, and that the effect of oxygen radicals is calmodulin dependent.

Animals↗