Department of Animal Science, Shahrekord University, Shahrekord, Iran.
Poult Sci. 2011 Jun;90(6):1287-94. doi: 10.3382/ps.2010-01120.
Methylglyoxal (MG) is a dicarbonyl molecule that forms during glycolysis and normally is detoxified via the glyoxalase system. Methylglyoxal is highly reactive with various amino acid residues in proteins, leading to oxidative stress and irreversible protein damage. Increased levels of MG have been associated with endothelial damage and vascular remodeling contributing to the development of systemic arterial hypertension in mammals. This study was conducted to determine whether administering exogenous MG can trigger pulmonary hypertension (increased pulmonary arterial pressure) in broilers. Hematological assays and preliminary mass spectrometric analyses also were conducted using blood samples from broilers that had been injected intramuscularly with either saline or MG to determine whether MG triggers either a toxic response or oxidative posttranslational modification of hemoglobin within 24 h postinjection. Clinically healthy male broilers received 100-µL intravenous injections of saline and then MG, followed by a 500-µL intramuscular injection. Neither intravenous nor intramuscular injections of saline altered the pulmonary arterial pressure, whereas both intravenous and intramuscular MG injections triggered pulmonary hypertension attributable to increased pulmonary vascular resistance. The precise mode of action by which MG triggers pulmonary vasoconstriction remains to be determined. Pulse oximetry, hematology, and matrix-assisted laser desorption ionization-time-of-flight spectra data did not provide evidence of an overt toxic response to MG, nor was modification of hemoglobin detected, although increased heterophil:lymphocyte ratios did demonstrate that MG caused a stress response. To the best of our knowledge the present results constitute the first demonstration in any vertebrate species that exogenously administered MG rapidly initiates pulmonary hypertension attributable to pulmonary vasoconstriction.
甲基乙二醛 (MG) 是一种二羰基分子，在糖酵解过程中形成，通常通过糖醛酸酶系统解毒。甲基乙二醛与蛋白质中的各种氨基酸残基高度反应，导致氧化应激和不可逆的蛋白质损伤。MG 水平的增加与内皮损伤和血管重塑有关，导致哺乳动物全身动脉高血压的发展。本研究旨在确定是否给予外源性 MG 可引发肉鸡的肺动脉高压（肺动脉压升高）。还使用肌肉内注射盐水或 MG 的肉鸡的血液样本进行了血液学测定和初步质谱分析，以确定 MG 是否在注射后 24 小时内引发血红蛋白的毒性反应或氧化翻译后修饰。接受过静脉注射生理盐水的临床健康雄性肉鸡随后接受 100-μL 静脉注射生理盐水，然后是 500-μL 肌肉内注射。盐水的静脉内和肌肉内注射均未改变肺动脉压，而静脉内和肌肉内 MG 注射均引发肺动脉高压，归因于肺血管阻力增加。MG 引发肺血管收缩的确切作用方式仍有待确定。脉搏血氧饱和度、血液学和基质辅助激光解吸电离飞行时间光谱数据未提供对 MG 产生明显毒性反应的证据，也未检测到血红蛋白修饰，尽管嗜中性粒细胞与淋巴细胞比值增加表明 MG 引起应激反应。据我们所知，目前的结果是在任何脊椎动物物种中首次证明外源性给予 MG 可迅速引发归因于肺血管收缩的肺动脉高压。
