Abstract
ABSTRACT Antioxidant systems like thioredoxin (Trx) and glutaredoxin (Grx) maintain oxidative stress balance. These systems have cross-talk supported by some in vitro studies. We investigated the underlying mechanisms of arsenic-induced liver injury in glutathione-deficient rats and whether there was any cross-talk between the Trx and Grx systems. The rats in arsenic-treated groups were administered with sodium arsenite (10, 20 mg/kg b w/d) for four weeks. In buthionine sulfoximine (BSO, an inhibitor of GSH) and 20 mg/kg arsenic combined groups, rats were injected with 2 mmol/kg BSO intraperitoneally twice per week. BSO exacerbated arsenic-induced liver injury by increasing arsenic accumulation in urine, serum, and liver while decreasing glutathione activity and resulting in upregulated mRNA expression of the Trx system and downregulation of Grx mRNA expression. The impact of Trx lasted longer than that of the Grx. The Trx system remained highly expressed, while GSH, Grx1, and Grx2 levels were decreased. The inhibitory effect of only BSO treatment on Grx1 and Grx2 was not pronounced. However, the combined impact of arsenic and BSO upregulated Trx expression, primarily related to further reduction of GSH. As a result, the suppressed Grxs were protected by the upregulated Trxs, which serve as a backup antioxidant defense system in the liver.
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