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Metabolic and Hematological Responses to Endotoxin-Induced Inflammation in Chicks Experiencing Embryonic 2,3,7,8-Tetrachlorodibenzodioxin Exposure.
Environmental Toxicology and Chemistry ( IF 3.6 ) Pub Date : 2020-07-29 , DOI: 10.1002/etc.4832
Lara Amaral-Silva 1, 2 , Hiroshi Tazawa 2 , Kênia Cardoso Bícego 1 , Warren W Burggren 2
Affiliation  

Dioxin exposure during bird embryonic development disrupts immunity as well as mechanisms involved in energy metabolism, potentially affecting negatively acute‐phase responses to pathogens. Thus, we hypothesized that embryonic exposure to 2,3,7,8‐tetrachlorodibenzodioxin (TCDD) changes the metabolism and blood physiology of domestic chicks, affecting their physiological competence for responding to immune challenges. To test this hypothesis, we injected doses of 0, 1.5, and 3 ng TCDD/egg (based on survival experiments) on embryonic day 4 and then measured O2 consumption and CO2 production for metabolic rate, ventilation, and body temperature (TB) in 5‐d‐old chicks. Then, chicks were injected with lipopolysaccharide (LPS, endotoxin) or saline prior to repeating the physiological measurements. A second chick group exposed to identical TCDD and LPS treatments had blood partial pressure of oxygen, partial pressure of carbon dioxide, pH, bicarbonate concentration, lactate concentration, osmolality, hemoglobin concentration, red blood cell concentration, and hematocrit, as well as TB, analyzed at 1 and 5 h after LPS injection. Metabolism in chicks embryonically exposed to 1.5 and 3 ng TCDD/egg was up to 37% higher, whereas body mass of chicks exposed to 3 ng TCDD/egg was approximately 6% lower. Chicks embryonically exposed to 3 ng TCDD/egg challenged with LPS showed a relative persistent hypometabolism accompanied by elimination of the normal hematological and osmotic responses to LPS. We conclude that embryonic exposure to TCDD affects posthatching metabolism as well as impairs metabolic, hematological, and osmotic responses to LPS. Environ Toxicol Chem 2020;39:2208–2220. © 2020 SETAC

中文翻译:

内毒素诱导的雏鸡发生胚胎2,3,7,8-四氯二苯并二恶英暴露的代谢和血液学对内毒素诱导的炎症反应。

鸟类胚胎发育过程中接触二恶英会破坏免疫力以及参与能量代谢的机制,可能会影响对病原体的负急性期反应。因此,我们假设胚胎暴露于2,3,7,8-四氯二苯并二恶英(TCDD)会改变家禽的代谢和血液生理,从而影响其应对免疫挑战的生理能力。为了检验这一假设,我们注射剂量的0,1.5和3纳克上4天胚胎TCDD /蛋(基于存活实验),然后测量的氧气2消耗和CO 2的生产的代谢速率,通风和体温(T)在5日龄的雏鸡中。然后,在重复生理测量之前,给小鸡注射脂多糖(LPS,内毒素)或盐水。接受相同TCDD和LPS处理的第二组雏鸡的血液氧分压,二氧化碳分压,pH,碳酸氢盐浓度,乳酸盐浓度,重量克分子渗透压浓度,血红蛋白浓度,红细胞浓度和血细胞比容以及T BLPS注射后1和5小时进行分析。胚胎暴露于1.5和3 ng TCDD /鸡蛋的雏鸡的代谢提高了37%,而暴露于3 ng TCDD /鸡蛋的雏鸡的体重降低了6%。雏鸡在暴露于3 ng TCDD /鸡蛋的情况下受到LPS攻击,表现出相对持续的低代谢,同时消除了对LPS的正常血液和渗透反应。我们得出的结论是,暴露于TCDD的胚胎会影响孵化后的代谢,并损害对LPS的代谢,血液学和渗透反应。2020年《环境毒理学》; 39:2208–2220。©2020 SETAC
更新日期:2020-07-29
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