title: Reciprocal effects of glucose on the process of cell death induced by calcium ionophore or H2O2 in rat lymphocytes.
abstract: We have examined the effects of glucose at high concentrations on the process of cell death induced by excessive increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) or oxidative stress in rat lymphocytes. The cell death elicited by the excessive increase in [Ca(2+)](i) seemed to be induced by an activation of Ca(2+)-dependent K(+) channels because the inhibitors for Ca(2+)-dependent K(+) channels attenuated the decrease in cell viability. Glucose at 30-50mM augmented the decrease in cell viability by the excessive increase in [Ca(2+)](i). It was not specific for glucose because it was the case for sucrose or NaCl, suggesting an involvement of increased osmolarity in adverse action of glucose. On the contrary, glucose protected the cells suffering from oxidative stress induced by H(2)O(2), one of reactive oxygen species. It was also the case for fructose or sucrose, but not for NaCl. The process of cell death induced by H(2)O(2) started, being independent from the presence of glucose. Glucose delayed the process of cell death induced by H(2)O(2). Sucrose and fructose also protected the cells against oxidative stress. The reactivity of sucrose to reactive oxygen species is lower than those of glucose and fructose. The order in the reactivity cannot explain the protective action of glucose. Glucose at high concentrations exerts reciprocal actions on the process of cell death induced by the oxidative stress and excessive increase in [Ca(2+)](i).
authors.affiliation: Laboratories of Cell Signaling and Bioorganochemistry, Faculty of Integrated Arts and Sciences, The University of Tokushima, Tokushima 770-8502, Japan.
authors.forename: Kanna
authors.initials: K
authors.lastname: Horimoto
authors.forename: Yumiko
authors.initials: Y
authors.lastname: Nishimura
authors.forename: Tomohiro M
authors.initials: TM
authors.lastname: Oyama
authors.forename: Kyoko
authors.initials: K
authors.lastname: Onoda
authors.forename: Hiroko
authors.initials: H
authors.lastname: Matsui
authors.forename: Toshihisa B
authors.initials: TB
authors.lastname: Oyama
authors.forename: Kaori
authors.initials: K
authors.lastname: Kanemaru
authors.forename: Toshiya
authors.initials: T
authors.lastname: Masuda
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Oyama
mesh_terms: D000818:Animals; D000001:Calcimycin / Q000633:toxicity*; D002118:Calcium / Q000378:metabolism; D016923:Cell Death; D002470:Cell Survival / Q000187:drug effects; D018999:Charybdotoxin / Q000633:toxicity; D003022:Clotrimazole / Q000633:toxicity; D004305:Dose-Response Relationship, Drug; D005434:Flow Cytometry; D005947:Glucose / Q000633:toxicity*; D006861:Hydrogen Peroxide / Q000633:toxicity*; D007476:Ionophores / Q000633:toxicity*; D008297:Male; D009994:Osmolar Concentration; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D013601:T-Lymphocytes / Q000187:drug effects* / Q000473:pathology
chemical_list: D007476:Ionophores; D018999:Charybdotoxin; D000001:Calcimycin; D006861:Hydrogen Peroxide; D003022:Clotrimazole; D005947:Glucose; D002118:Calcium