Rajashree S, Puvanakrishnan R
Department of Biotechnology, Central Leather Research Institute, Adyar, Madras, India.
Mol Cell Biochem. 1998 Apr;181(1-2):77-85. doi: 10.1023/a:1006833824163.
This study was designed to investigate the alterations in thiobarbituric acid reactants (TBA-reactants) and enzymatic and nonenzymatic antioxidant levels induced by dexamethasone (Dex) in heart and kidney and to find out whether these alterations induced by Dex and its hypertensive effect had any role in the maintenance of hypertension in this model. Administration of dexamethasone induced severe loss of body weight, significant increase in heart and kidney weights and also marked electrocardiographic changes. The protein content in heart and kidney increased significantly during Dex administration and returned to near normalcy after withdrawal. Total activity of lactate dehydrogenase showed a significant increase in heart till day 8 of treatment, whereas in serum, it exhibited a significant decrease. The activity of CK in heart showed an increase till day 8 of treatment and approached normalcy thereafter. In serum, CK exhibited a decrease till day 8, remaining insignificant thereafter. CKMB in heart showed an insignificant increase initially, reaching normal levels on Dex withdrawal, whereas in serum, it showed a significant decrease throughout the experimental period. Mean arterial pressure (MAP) and heart rate increased significantly, while a significant elevation in the ST segment was noticed during administration as well as after withdrawal of Dex. The TBA-reactants levels were found to increase in heart and kidney during days 12 and 16 of administration with Dex and even after withdrawal of Dex, the levels were insignificantly elevated. The level of glutathione in heart and kidney increased from day 4 onwards and reached normalcy during the later stages of treatment and after withdrawal of Dex. The total sulfhydryl groups exhibited a significant increase in both heart and kidney throughout the experiment. The antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase and glutathione S-transferase exhibited a significant decrease in heart during Dex administration whereas, in kidney, they exhibited a significant increase during treatment and after withdrawal of Dex. Thus, Dex induced rise in mean arterial pressure, significant alterations in electrocardiographic parameters and also marked alterations in enzymatic and nonenzymatic antioxidant levels and in the TBA-reactants level in heart and kidney.
本研究旨在调查地塞米松(Dex)诱导的心、肾中硫代巴比妥酸反应物(TBA反应物)以及酶促和非酶促抗氧化剂水平的变化,并探究Dex诱导的这些变化及其高血压效应在该模型中高血压维持过程中是否发挥作用。给予地塞米松导致体重严重减轻、心、肾重量显著增加以及明显的心电图变化。在给予Dex期间,心、肾中的蛋白质含量显著增加,停药后恢复至接近正常水平。乳酸脱氢酶的总活性在治疗至第8天时心脏中显著增加,而在血清中则显著降低。心脏中肌酸激酶(CK)的活性在治疗至第8天时增加,此后接近正常水平。在血清中,CK在第8天之前降低,此后保持不显著水平。心脏中的肌酸激酶同工酶(CKMB)最初增加不显著,在停用Dex时达到正常水平,而在血清中,其在整个实验期间显著降低。平均动脉压(MAP)和心率显著增加,在给予Dex期间以及停药后均观察到ST段显著升高。在给予Dex的第12天和第16天以及停药后,心脏和肾脏中的TBA反应物水平均升高,且停药后水平仍有不显著升高。心脏和肾脏中的谷胱甘肽水平从第4天开始增加,并在治疗后期和停药后恢复正常。在整个实验过程中,心脏和肾脏中的总巯基均显著增加。抗氧化酶如过氧化氢酶、超氧化物歧化酶、谷胱甘肽过氧化物酶和谷胱甘肽S-转移酶在给予Dex期间心脏中显著降低,而在肾脏中,它们在治疗期间和停药后显著增加。因此,Dex导致平均动脉压升高、心电图参数显著改变,以及心脏和肾脏中酶促和非酶促抗氧化剂水平及TBA反应物水平显著改变。