Optical imaging of mitochondrial redox state in rodent models with 3-iodothyronamine.
Optical imaging of mitochondrial redox state in rodent models with 3-iodothyronamine.
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DOI：
10.1177/1535370213510252
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发表时间：
2014-02
期刊：
影响因子：
--
通讯作者：
Ranji M
中科院分区：
文献类型：
--
作者：
Ghanian Z;Maleki S;Reiland H;Bütz DE;Chiellini G;Assadi-Porter FM;Ranji M
本研究使用光学技术测量低剂量 (10 mg/kg) 和高剂量 (25 mg/kg) 3-碘甲腺胺 (T1AM) 对小鼠肾脏和心脏代谢的影响。组织中两个固有荧光团的比率 (NADH/FAD)，称为 NADH 氧化还原比 (NADH RR)，是组织代谢状态的标志。使用冷冻荧光成像仪器对接受 3-碘甲腺胺处理的小鼠的肾脏和心脏中的 NADH RR 进行定量评估。我们将这些结果与对照小鼠的相应组织进行了比较。在用高剂量 T1AM 治疗的小鼠肾脏中，NADH RR 最大预测平均值为 2.6 ± 0.6，而对照小鼠为 3.20 ± 0.03，表明高剂量治疗的肾脏中氧化应激 (OS) 显着增加了 19% (± 0.4) (P=0.047)。然而，与对照小鼠的肾脏相比，用低剂量 T1AM 处理的肾脏显示 NADH RR 没有差异。此外，低剂量与高剂量 T1AM 治疗在心脏和肾脏中显示出不同的反应。对于低剂量和高剂量 T1AM 治疗的小鼠，心脏中 NADH RR 最大投影的平均值分别从 3.0 ± 0.3 变为 3.2 ± 0.6，而对照组小鼠为 2.8 ± 0.7。这些值对应于 T1AM 处理的心脏中 NADH RR 显着增加 9% (±0.5) (P=0.045) 和 14% (±0.5) (P=0.008)，表明与低剂量处理的组织或对照组织相比，高剂量 T1AM 处理的组织 OS 降低。这些结果表明，虽然高剂量的 T1AM 会增加肾脏的氧化反应，但它对心脏具有保护作用，并且可能通过不同剂量和组织特定水平的替代途径发挥其作用。
This study used an optical technique to measure the effects of treating low (10 mg/kg) and high (25 mg/kg) doses of 3-iodothyronamine (T1AM) on the metabolism in the kidney and heart of mice. The ratio of two intrinsic fluorophores in tissue, (NADH/FAD), called the NADH redox ratio (NADH RR), is a marker of the metabolic state of the tissue. A cryofluorescence imaging instrument was used to provide a quantitative assessment of NADH RR in both kidneys and hearts in mice treated with 3-iodothyronamine. We compared those results to corresponding tissues in control mice. In the kidneys of mice treated with a high dose T1AM, the mean values of the maximum projection of NADH RR were 2.6 ± 0.6 compared to 3.20 ± 0.03 in control mice, indicating a 19% (± 0.4) significant increase in oxidative stress (OS) in the high dose-treated kidneys (P=0.047). However, kidneys treated with a low dose of T1AM showed no difference in NADH RR compared to the kidneys of control mice. Furthermore, low versus high dose treatment of T1AM showed different responses in the heart than in the kidneys. The mean value of the maximum projection of NADH RR in the heart changed from 3.0 ± 0.3 to 3.2 ± 0.6 for the low dose and the high dose T1AM-treated mice, respectively, as compared to 2.8 ± 0.7 in control mice. These values correspond to a 9% (±0.5) (P=0.045) and 14% (±0.5) (P=0.008) significant increase in NADH RR in the T1AM-treated hearts, indicating that the high dose T1AM-treated tissues have reduced OS compared to the low dose-treated tissues or the control tissues. These results suggest that while T1AM at a high dose increases oxidative response in kidneys, it has a protective effect in the heart and may exert its effect through alternative pathways at different doses and at tissue specific levels.
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