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首页> 外文期刊>Toxicology Letters: An International Journal Providing a Forum for Original and Pertinent Contributions in Toxicology Research >Water metabolism dysfunction via renin-angiotensin system activation caused by liver damage in mice treated with microcystin-RR
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Water metabolism dysfunction via renin-angiotensin system activation caused by liver damage in mice treated with microcystin-RR

机译：用微囊杆菌 - RR处理的小鼠肝损伤引起的肾素 - 血管紧张素系统活化的水代谢功能障碍

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摘要

Microcystins (MCs) are a group of monocyclic heptapeptide toxins that have been shown to act as potent hepatotoxins. However, the observed symptoms of water metabolism disruption induced by microcystin-RR (MC-RR) or MCs have rarely been reported, and a relatively clear mechanism has not been identified. In the present study, male mice were divided into 4 groups (A: 140 mu g/kg, B: 70 mu g/kg, C: 35 mu g/kg, and D: 0 mu g/kg) and administered MC-RR daily for a month. On day 8 of treatment, an increase in water intake and urine output was observed in the high-dose group compared with the control, and the symptoms worsened with the repeated administration of the toxin until day 30. In addition, the urine specific gravity decreased and serum enzymes that can reflect hepatic damage increased in the high-dose group compared with the control (P < 0.05). The mRNA level of angiotensinogen (AGT) in hepatocytes was upregulated to approximately 150% of the control (P < 0.05), and the serum renin-angiotensin system (RAS) was activated in the high-dose group; however, signs of renal injury were not observed throughout the experiment. After the toxin treatment was completed, the high levels of the RAS and vasopressin in group A returned to normal levels within 1 week. As expected, the symptoms of polyuria and polydipsia also disappeared. Therefore, we propose that water metabolism dysfunction occurs via RAS activation caused by liver damage because the increased serum RAS levels in the experiment were consistent with the increased urine output and water intake in the mice during the observation period. In addition, we found for the first time that a RAS blocker could alleviate the observed polyuria and polydipsia and inactivate the high level of the RAS induced by MC-RR in a dose-dependent manner, which further supported our hypothesis.
机译：微囊藻（MCS）是一组已显示用作充当肝毒素的单环庚肽毒素。然而，很少报道通过微阴压-RR（MC-RR）或MCS诱导的水代谢破坏的观察到的水代谢破坏的症状，并且尚未确定相对清晰的机制。在本研究中，将雄性小鼠分成4组（A：140μg/ kg，b：70μg/ kg，c：35μg/ kg和d：0μg/ kg）并施用mc- RR每月一个月。在第8天的治疗中，与对照相比，在高剂量组中观察到水摄入量和尿液产量的增加，并随着毒素的反复施用症状，直到30天。此外，尿液比重力减少与对照相比，高剂量组可以反映肝损伤的血清酶（P <0.05）。肝细胞中血管紧张素（AGT）的mRNA水平上调至约150％的对照（P <0.05），并且在高剂量组中激活血清肾素 - 血管紧张素系统（RAS）;然而，在整个实验中未观察到肾损伤的迹象。完成毒素处理后，A组中的RAS和血管加压素在1周内恢复到正常水平。正如预期的那样，聚需要的症状和较多潜水脂肪也消失了。因此，我们提出通过肝脏损伤引起的Ras活化发生水代谢功能障碍，因为在观察期间，实验中的血清RAS水平的增加一致地与小鼠的尿量增加和水摄入量一致。此外，我们首次发现了RAS阻滞剂可以缓解观察到的聚尿和较益级脂肪，并以剂量​​依赖的方式灭活MC-RR诱导的高水平RAS，这进一步支持了我们的假设。

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