首页> 美国卫生研究院文献>Oxidative Medicine and Cellular Longevity >In Vivo Effects of Vanadium Pentoxide and Antioxidants (Ascorbic Acid and Alpha-Tocopherol) on Apoptotic Cytotoxic and Genotoxic Damage in Peripheral Blood of Mice
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In Vivo Effects of Vanadium Pentoxide and Antioxidants (Ascorbic Acid and Alpha-Tocopherol) on Apoptotic Cytotoxic and Genotoxic Damage in Peripheral Blood of Mice

机译:五氧化二钒和抗氧化剂(抗坏血酸和α-生育酚)对小鼠外周血细胞凋亡细胞毒性和遗传毒性的体内作用

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摘要

This study was conducted to investigate the effects of vanadium pentoxide (V2O5), ascorbic acid (AA), and alpha-tocopherol (α-TOH) on apoptotic, cytotoxic, and genotoxic activity. Groups of five Hsd:ICR mice were treated with the following: (a) vehicle, distilled water; (b) vehicle, corn oil; (c) AA, 100 mg/kg intraperitoneally (ip); (d) α-TOH, 20 mg/kg by gavage; (e) V2O5, 40 mg/kg by ip injection; (f) AA + V2O5; and (g) α-TOH + V2O5. Genotoxic damage was evaluated by examining micronucleated polychromatic erythrocytes (MN-PCE) obtained from the caudal vein at 0, 24, 48, and 72 h after treatments. Induction of apoptosis and cell viability were assessed at 48 h after treatment in nucleated cells of peripheral blood. Treatment with AA alone reduced basal MN-PCE, while V2O5 treatment marginally increased MN-PCE at all times after injection. Antioxidants treatments prior to V2O5 administration decreased MN-PCE compared to the V2O5 group, with the most significant effect in the AA + V2O5 group. The apoptotic cells increased with all treatments, suggesting that this process may contribute to the elimination of the cells with V2O5-induced DNA damage (MN-PCE). The necrotic cells only increased in the V2O5 group. Therefore, antioxidants such as AA and α-TOH can be used effectively to protect or reduce the genotoxic effects induced by vanadium compounds like V2O5.
机译:进行了这项研究,以研究五氧化二钒(V2O5),抗坏血酸(AA)和α-生育酚(α-TOH)对细胞凋亡,细胞毒性和基因毒性的影响。每组五只Hsd:ICR小鼠用以下药物处理:(a)溶媒,蒸馏水; (b)车辆,玉米油; (c)AA,腹膜内(ip)100µmg / kg; (d)α-TOH,管饲法为20μg/ kg; (e)经腹腔注射V2O5,40µmg / kg; (f)AA + V2O5; (g)α-TOH+ V2O5。通过检查治疗后0、24、48和72 h从尾静脉获得的微核多色红细胞(MN-PCE)来评估遗传毒性损害。在外周血的有核细胞中处理后48小时,评估凋亡的诱导和细胞活力。单独使用AA的治疗可减少基础MN-PCE,而V2O5治疗在注射后的所有时间均略微增加MN-PCE。与V2O5组相比,V2O5给药前的抗氧化剂治疗降低了MN-PCE,在AA + V2O5组中效果最为显着。所有处理均导致凋亡细胞增加,提示该过程可能有助于消除V 2 O 5 诱导的DNA损伤(MN-PCE)的细胞。坏死细胞仅在V 2 O 5 组中增加。因此,抗氧化剂如AA和α-TOH可有效地保护或降低钒化合物V 2 O 5 引起的遗传毒性作用。

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