Oxidative Stress in the in vivo DMBA Rat Model of Breast Cancer: Suppression by a Voltage-gated Sodium Channel Inhibitor (RS100642)
Oxidative Stress in the in vivo DMBA Rat Model of Breast Cancer: Suppression by a Voltage-gated Sodium Channel Inhibitor (RS100642)
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DOI：
10.1111/j.1742-7843.2012.00880.x
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发表时间：
2012-08-01
影响因子：
3.1
通讯作者：
Djamgoz, Mustafa B. A.
中科院分区：
文献类型：
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作者：
Batcioglu, Kadir;Uyumlu, A. Burcin;Djamgoz, Mustafa B. A.
用7，12-二甲基苯并蒽（DMBA）诱发雌性大鼠乳腺癌（BCa）。讨论了两个主要问题。首先，致癌过程是否伴随着氧化应激，如超氧化物歧化酶、谷胱甘肽过氧化物酶、丙二醛和总硝酸盐所示？其次，是否会额外治疗大鼠与电压门控钠通道（VGSC）的活动，以前显示，以促进BCa的进展，影响氧化反应？DMBA诱导的抗氧化系统的增加被VGSC抑制剂RS 100642完全阻断，这也显着延长了寿命。我们的结论是，VGSC抑制在体内可以显着保护免受氧化应激和提高生存从肿瘤负荷。
Breast cancer (BCa) was induced in vivo in female rats with 7,12-dimethylbenz(a)anthracene (DMBA). Two main questions were addressed. Firstly, would the carcinogenesis be accompanied by oxidative stress as signalled by superoxide dismutase, glutathione peroxidase, malondialdehyde and total nitrate? Secondly, would treating the rats additionally with a blocker of voltage-gated sodium channel (VGSC) activity, shown previously to promote BCa progression, affect the oxidative responses? The DMBA-induced increases in the antioxidant systems were completely blocked by the VGSC inhibitor RS100642, which also significantly prolonged the lifespan. We conclude that VGSC inhibition in vivo can significantly protect against oxidative stress and improve survival from tumour burden.