十甲氧胺作用下淋巴细胞抗氧化和no合酶系统的特性

I. Kovalenko, O. K. Onufrovych, R. Fafula, O. Melnyk, Z. Vorobets, Danylo Halytskyi
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引用次数: 0

摘要

抗菌药物主要对皮肤表面、粘膜、伤口表面和体腔有杀微生物作用。十甲氧嘧啶是一种化合物[1,10 -十甲氧基二(N, N -二甲基甲氧基羰基甲基)二氯化铵],对革兰氏阳性(葡萄球菌、链球菌、肺炎球菌)、革兰氏阴性(淋球菌、脑膜炎球菌)球菌、白喉粘连菌、肠细菌、假单胞菌、原生动物、皮肤真菌、酵母菌属类酵母菌、衣原体和病毒具有广泛的抗菌作用。当炎症过程和病理状况主要由调节系统的破坏、脂质过氧化过程的激活和抗氧化保护系统的破坏引起时,发生在身体细胞中的病理过程。由于十甲氧胺具有亲水性和亲脂性,可通过创面、粘膜、皮肤等渗透到细胞、血液中,并经血液传递到不同的器官和组织,从而引起多种生化作用,特别是对细胞的调节性no -合成酶系统。在这方面,十甲氧苄啶对细胞的生物学作用,特别是血液淋巴细胞。它激活谷胱甘肽抗氧化系统的酶,刺激精氨酸酶的活性,抑制NO合成酶的组成异构体的活性,同时激活NO合成酶的诱导异构体。
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Characteristics of antioxidant and NO-synthase systems of blood lymphocytes under the action of decamethoxine
Antiseptic drugs have mostly microbicidal effect on the skin surface, mucous membranes, surfaces of a wound and body cavities. Decamethoxine is a chemical compound [1, 10-decameth-ylene bis (N, N – dimethylmethoxycarbonylmethyl) ammonium dichloride] that has a wide range of antimicrobial actions on Gram - positive (staphylococcus, streptococcus, pneumococcus), Gram-negative (gonococcus, meningococcus) cocci, diphtheria corynebacteria, enterobacteria, pseudomonads, protozoa, dermatophytes, yeasts-like fungi of the genus Candida , chlamydia and viruses. Pathological processes that occur in the cells of the body when inflammatory processes and pathological conditions are caused primarily by the violation of regulatory systems, the activation of lipid peroxidation processes and the violation of antioxidant protective system. Since decamethoxine has hydrophilic and lipophilic properties, it can penetrate into cells, blood through surfaces of a wound, mucous membranes, skin, etc., and be transmitted by blood to different organs and tissues, thus causing a variety of biochemical effects, particularly regarding to the regulatory NO-synthase system of cells. In this respect the biological action of decamethoxine nisms of the cell, blood lymphocytes in particular. It activates the enzymes of the glutathione antioxidant system, stimulates the activity of arginase and inhibits the activity of the constitutive isoform of NO synthase with the simultaneous activation of the inducible isoform of NO synthase.
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