• Korean Journal of Environmental Biology
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• v.19 no.2
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• pp.147-152
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• 2001

Whether the pretreatment of sublethal arsenic or cadmium may prevent from lethality of arsenic or cadmium to mice, respectively, and also the protection against to lethality of arsenic or cadmium which might be induced by pretreatment of arsenic or cadmium may be related with their hepatic glutathione contents were investigated. When sodium arsenite or cadmium chloride was subcutaneously injected to mice (ICR strain) using lethal doses, all mice of both group were killed. The mortality of mice which were subsequently injected with lethal arsenic 24 hours after pretreatment of sublethal arsenic was decreased, and the same result was obtained in the case of cadmium. Sublethal pretreatment of arsenic or cadmium prior to lethal arsenic or cadmium treatment to mice, respectively, didn't decrease hepatic glutathione contents of the survived mice, while decreases of that contents in liver were observed in the mice just after they died. Cadmium pretreatment decreased mortality of mice which subsequently injected with lethal arsenic, while arsenic pretreatment didn't protect against cadmium lethality. These results indicate that protection against arsenic or cadmium lethality to mice induced by pretreatment of sublethal arsenic or cadmium may be directly related to other factors induced by sublethal camium pretreatment, not to hepatic glutathione contents.

• BMB Reports
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• v.31 no.1
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• pp.83-88
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• 1998

Recently a B cell surface molecule, CD40, has emerged as a receptor mediating a co-stimulatory signal for B cell proliferation and differentiation. To investigate the mechanism of synergy between interleukin-4 (IL-4) and CD40 ligation in B cell activation, we have examined the effect of CE40 cross-linking on the IL-4 receptor expression in human B cells using anti-CE40 antibody. We observed that IL-4 and anti-CD40 both induce IL-4 receptor gene expression with a rapid kinetics resulting in a noticeable accumulation of IL-4 receptor mRNA within 4 h. While IL-4 caused a dose-dependent induction of surface IL-4 receptor expression, the inclusion of anti-CD40 in the IL-4-treated culture, further up-regulated the IL-4-induced IL-4 receptor expression as analyzed by flow cytometry. Pretreatment of B cells with inhibitors of protein tyrosine kinase (PTK) resulted in a significant inhibition of both the IL-4- and anti-CD40-induced IL-4 receptor mRNA levels, while protein kinase C (PKC) inhibitors had no effects. These results suggest that IL-4 and CD40 ligation generate B cell signals, which via PTK-dependent pathways, lead to the synergistic induction of IL-4 receptor gene expression. The rapid induction of IL-4 receptor gene expression through the tyrosine kinase-mediated signal transduction by B cell activating stimuli, would provide cells capacity for an efficient response to IL-4 in the early phase of IL-4 action, and may in part constitute the molecular basis of the reported anti-CD40 co-stimulatory effect on the IL-4-induced response.