In vivo effects of methamphetamine on brown fat reactive oxygen species and mitochondria.
In vivo effects of methamphetamine on brown fat reactive oxygen species and mitochondria.
复制标题
甲基苯丙胺对棕色脂肪活性氧和线粒体的体内影响。
DOI：
10.1080/23328940.2015.1091874
复制
发表时间：
2015
期刊：
影响因子：
--
通讯作者：
Marcondes,MariaCeciliaGaribaldi
中科院分区：
文献类型：
--
作者：
Bortell,Nikki;Najera,JuliaA;Sanchez-Alavez,Manuel;Marcondes,MariaCeciliaGaribaldi
甲基苯丙胺（俗称冰毒）是一种高度成瘾的滥用药物，它会导致核心体温或体温过高的潜在致命增加。我们最近发现，Meth-induced体温过高有显着的产热棕色脂肪组织的参与，1，可以通过预处理与抗氧化剂N-乙酰半胱氨酸预防。1在本出版物中，我们通过向C57 Bl/6小鼠注射二氢乙锭，在体内标记活性氧，如超氧化物;然后收获并处理肩胛间棕色脂肪组织（方法见参考文献1）。在棕色脂肪中观察到活性氧，发现其主要与线粒体相关（幻灯片1）。在载玻片中，二氢乙锭标记的超氧化物显示为红色;线粒体标记物TOMM 20显示为黄色;细胞骨架F-肌动蛋白标记物鬼笔环肽Alexa 488显示为绿色; DNA标记物DAPI显示为蓝色。甲基耗尽超氧化物在棕色脂肪线粒体，与TOMM 20标记的线粒体的损失。早在注射药物后15分钟就可在棕色脂肪中检测到这些变化，在注射后1小时达到峰值，见载玻片1。N-乙酰半胱氨酸预处理防止了由甲基诱导的TOMM 20的损失，但没有恢复线粒体中的甲基耗尽的超氧化物储存。总的来说，这张幻灯片显示，甲基影响线粒体储存的超氧化物，以及线粒体的完整性，在棕色脂肪组织。这些观察结果的功能重要性仍有待确定，需要进一步研究。
Methamphetamine (commonly known as Meth) is a highly addictive drug of abuse, which causes a potentially lethal increase in core body temperature, or hyperthermia. We have recently found that Meth-induced hyperthermia has a significant participation of the thermogenic brown adipose tissue, 1 and can be prevented by a pretreatment with the antioxidant N-acetyl cysteine. 1 For this publication, we labeled reactive oxygen species, such as superoxide, in vivo, by injecting C57Bl/6 mice with dihydroethidium; we then harvested and processed interscapular brown adipose tissue (for methods, see ref. 1). Reactive oxygen species were visualized in brown fat and found to be largely associated with mitochondria (Slide 1). In the slide, dihydroethidium-labeled superoxide is seen as red; the mitochondrial marker TOMM20 is seen as yellow; the cytoskeleton F-actin marker Phalloidin Alexa488 is seen as green; and the DNA marker DAPI is seen in blue. Meth depleted superoxide in brown-fat mitochondria, in correlation with the loss of TOMM20-labeled mitochondria. These changes were detectable in brown fat as early as 15 minutes after the injection of the drug, with a peak at1 hour following injection, which is seen in Slide 1. The N-acetyl cysteine pretreatment prevented the loss of TOMM20 induced by Meth, but did not restore the Meth-depleted superoxide storages in mitochondria. Overall, this slide shows that Meth impacts the mitochondrial storages of superoxide, as well as mitochondrial integrity, in brown adipose tissue. The functional importance of these observations remains to be established and requires further studies.