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In sum, the safety observations support the concept that the IRR, the target of ARA 290, is induced only by injury, inflammation or metabolic stress and is therefore not generally expressed by normal tissues, thus limiting systemic adverse events

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In rat hepatocytes, NO exerted no influence on the basal GSH level or GCL expression but was involved in up-regulating GCL expression in response to IL-1 (Kuo et al., 1996)