Activities of heme oxygenase and tryptophan-2,3-dioxygenase and cytochrome P450 content in liver as well as absorption of the Soret band and optical density at 280 nm in serum were determined 2 and 24 h after administration of HgCl(2) and CoCl(2) and after co-administration of the metal salts with alpha-tocopherol. Administration of HgCl(2) and CoCl(2) increased the contents of hemolysis products in the serum, induced heme oxygenase, and decreased cytochrome P450 content in the liver. Injection of HgCl(2) increased the activity of tryptophan-2,3-dioxygenase holoenzyme and enzyme saturation with the heme, but administration of CoCl(2) decreased these parameters. Pretreatment with alpha-tocopherol completely blocked the changes induced by HgCl(2) after 24 h. Induction of heme oxygenase induced by CoCl(2) was not blocked by alpha-tocopherol, but this antioxidant normalized the increase in the level of hemolysis products in the serum and decrease in tryptophan-2,3-dioxygenase holoenzyme activity and cytochrome P450 content. Mechanisms of regulation of heme oxygenase by mercury and cobalt ions are discussed.
Heme distribution in subcellular fractions of rat liver was studied first hours under the action of several agents causing oxidative stress in vivo. Total and post-mitochondrial heme content in liver was found to depend on both the level of hemolysis products in blood and agent's capacity to modify heme and hemoproteins. The increase of activity of 5-aminolevulinate synthase (ALAS) and/or heme accumulation in mitochondria was accompanied by increase of tryptophan-2,3-dioxygenase (TDO) heme saturation. Membrane stabilisation by tocopherol or prevention of early ALAS induction by cycloheximide prevented both mitochondrial heme accumulation and increase of TDO heme saturation. Modification of heme fully prevented the alterations of total heme content even under severe hemolysis as well as the increase of TDO heme saturation if no increase of heme synthesis occurred. Thus heme synthesis can greatly contribute to heme intracellular redistribution under oxidative stress.
The purpose of the study is to evaluate the content of IL‑7, –4 and –17A in the blood of patients with psoriasis, depending on the severity of the disease. Materials and methods. A group of patients was examined, which included 47 patients with vulgar psoriasis; 10 patients with arthropathic psoriasis, as well as a control group of 15 conditionally healthy individuals. The content of interleukin –4, –7, –17A was determined in blood serum by the immunoenzymatic method. Results and conclusions. In patients with a severe course of psoriasis (arthropathic psoriasis), pathological activation of hereditary and acquired (Th1- and Th17-types) immunity is observed, there is a dysregulation of the synthesis of pro-inflammatory (IL‑17) and anti-inflammatory (IL‑4) cytokines. Detection of disturbances in the levels of mediators of the immune response, which are involved in the formation of immune inflammation, in particular cytokines, in patients with psoriasis can serve as an additional test for predicting the clinical course of this dermatosis.
The aim is to study the state of indicators of oxidative modification of proteins in the blood plasma of patients with psoriasis vulgaris. Materials and Methods. 18 patients with psoriasis vulgaris (average age – 44.4 years) and a group of healthy donors – 22 persons, who made up the control group – were examined. Oxidative modification of proteins was determined in blood plasma by reaction with 2,4-dinitrophenylhydrazine. Results In patients with psoriasis vulgaris, significant violations of the processes of oxidative modification of blood plasma proteins (spontaneous and metal-catalyzed) were detected. Conclusions. In patients with psoriasis vulgaris, the period of exacerbation of the disease, is accompanied by carbonyl stress, which is confirmed by a significant increase in the blood content of aldehyde and ketone phenylhydrazones.
The article presents literature data on the study of the content of pro- and anti-inflammatory cytokines in psoriasis and their relationship with the activity of the dermatological pathological process. Cytokines play one of the key roles in the development and maintenance of psoriatic lesions. Processes that are accompanied by pathological changes in lymphocytes, neutrophils, keratinocytes, endothelial and other cells in psoriasis are induced by the combined effects of many cytokines, chemokines, and other mediators of inflammation. It is possible that an imbalance in the system of pro- and anti-inflammatory cytokines of systemic and local origin may play a key role in this pathology.
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