RCAN1 is an inhibitor of the phosphatase calcineurin, which is involved in the regulation of oxidative stress and apoptosis, among other important cell processes. Here we have used RCAN1 deficient mice (RCAN1^-/-) to elucidate its role after an acute oxidative insult such as paraquat injection. We have observed that RCAN1^-/- mice show less oxidative damage than wildtype (WT) mice after treatment. Under basal conditions, RCAN1^-/- animals express more calcineurin, heme oxygenase-1, Nrf2, and catalase compared to WT mice (controls). This may explain the less severe effect of paraquat treatment on RCAN1^-/- mice compared to WT. We showed that oxidative stress is involved in the early stages of apoptosis, thus we determined the apoptotic effector BAD and found that decreases in RCAN1^-/- mice after treatment with paraquat compared with WT in similar experimental conditions. Our results suggest that RCAN1 may be involved in the balance between oxidant and antioxidant species production in vivo.

RCAN1是磷酸钙调磷酸酶的抑制剂，磷酸钙调磷酸酶在其他重要的细胞过程中参与氧化应激和细胞凋亡的调节。在这里，我们使用了RCAN1缺陷小鼠（RCAN1 ^-/-）来阐明其在急性氧化损伤（例如百草枯注射液）后的作用。我们已经观察到，RCAN1 ^-/-小鼠在治疗后显示出比野生型（WT）小鼠更少的氧化损伤。在基础条件下，与WT小鼠（对照）相比，RCAN1 ^-/-动物表达更多的钙调神经磷酸酶，血红素加氧酶-1，Nrf2和过氧化氢酶。这可以解释百草枯对RCAN1的不良影响^-/-小鼠相比WT。我们显示氧化应激参与细胞凋亡的早期阶段，因此我们确定了凋亡效应因子BAD，并且在相似的实验条件下，百草枯处理后的RCAN1 ^-/-小鼠相比WT减少了。我们的结果表明，RCAN1可能参与体内氧化剂和抗氧物质产生之间的平衡。