Proper functioning of homeostatic mechanisms is characteristic for every healthy organism and enables adapting to environmental changes. These complicated systematic reactions can neutralize the harmful stress factors leading to various inflammatory reactions. The aim of this study was to determine dynamic changes in the inflammatory reaction after single 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) administration of 5 μg/kg body weight into rats with experimentally induced pleuritis. These changes were observed by monitoring the hematological blood parameters during inflammation. The obtained results proved that dioxins contribute to various changes in the character of the inflammatory response. TCDD administration before pleuritis initiation caused an increase of lymphocytes and significant decrease of the number of neutrophils during inflammation. The current study proved that administration of low TCDD dose (seven times lower than used in other studies) can cause thymus, spleen, or lymphatic gland atrophy. This finding indicates the toxic influence of small TCDD dose especially on the immune system.

The aim of this study was to evaluate the effect of tocopherol on pleuritis-induced rats exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Rats were treated with a single TCDD dose of 5 μg/kg body weight (b.w.) and then for 3 weeks they were daily supplemented with tocopherol at a dose of 30 mg/kg b.w. The inflammation was initiated by intrapleural injection of a single dose of 1% carrageenin solution in a volume of 0.15 ml. Changes in biochemical blood parameters were measured three times at the 24th, 72nd and 120th hour of pleuritis and the blood was collected from 20 animals of each group of rats (group with the control inflammation; group treated with TCDD and with control inflammation; group treated with TCDD, supplemented with tocopherol and with the inflammation). The following biochemical parameters were measured: tumor necrosis factor (TNF), interleukin-1 (IL-1), IL-2, IL-4, IL-6, procollagen, telopeptide, fibrinogen, cholesterol, urea, creatinine, aspartate aminotransferase (AspAT) and alanine aminotransferase (AlAT). Daily supplementation of tocopherol caused significant changes in the level of TNF, IL-1, IL-4, IL-6, urea, creatinine, AspAT and AlAT. According to the results of these studies, we suggest that tocopherol supplementation in high doses could act as a protective treatment to improve liver metabolism.

A significant role is played in inflammation by the liver, which, stimulated by inflammatory mediators, synthetizes plasma proteins with various dynamics. The purpose of these studies is to generate a detailed dynamic analysis of changes to concentrations of plasma and serum protein fractions and selected acute-phase proteins as well as nonspecific biochemical indices during the course of an induced pleurisy. The studies were conducted on female inbred Buffalo rats, which were divided into two groups: a control group (C) and an experimental group (IP) in which pleurisy was induced. In the IP group, significant changes in biochemical indices were observed between the 48th and 96th hours of pleurisy. A reduction of albumin, transferrin, urea, and creatinine concentrations was observed, while concentrations of the complement components C3 and C4, haptoglobin, and fibrinogen increased. An early increase of IL-1 was observed, while increases of IL-6 and TNF were noted in the later period. The maximum intensity of the processes described above occurred between the 72nd and 96th hours of pleurisy.

Toxicity of dioxins is wide ranging. Amongst the organs, the liver is the most susceptible to damage by dioxins. Damage caused to liver cells results in promoting inflammatory processes. The aim of this work was to evaluate whether high doses of tocopherol will change the inflammatory response, monitored by biochemical indicators, by improving liver function in rats exposed to tetrachlorodibenzo-p-dioxin (TCDD). The study was conducted on a population of female Buffalo rats. The animals were divided into the following groups: Control Group A—representing physiological norms for the studied diagnostic indicators; Control Group B—subjects were administered a 1% ceragenin solution to induce pleuritis; Study Group 1—where rats were administered α-tocopherol acetate for 3 weeks, after which pleuritis was induced; Study Group 2—rats were administered a single dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), while 3 weeks later, pleuritis was induced; and Study Group 3—rats were administered a single dose of TCDD and next, were administered α-tocopherol acetate for 3 weeks, followed by pleuritis induction. The results clearly show that administering tocopherol in the course of inflammation causes changes to the distribution and ratio of in the serum protein fractions, including acute phase proteins. The latter proteins are indicative to the improvement in liver function and linked to protein synthesis and stimulation of the antibody-mediated immunity. Moreover, in the course of inflammation caused by exposure of rats to TCDD, tocopherol significantly affected the acute phase protein concentration.

The results suggest that nitrogranulogen affects the erythropoiesis.