[The influence of methionine and vitamin E on oxidative stress in rats' liver exposed to sodium fluoride] / Wplyw metioniny i witaminy E na stres oksydacyjny oceniany w watrobie szczurów narazonych na dzialanie fluorku sodu

BACKGROUND: Fluorine influences many processes occurring in the organism. Controversies over the evaluation of the biological effects of this substance are due to a small difference between tolerable and toxic fluorine doses. One of the main mechanisms of the fluorine toxic action is its ability to induce oxidative stress via reactive oxygen species generation and antioxidant defense system impairment. It is important to evaluate possible interactions between fluorine and other substances that may increase or decrease its toxicity. MATERIAL AND METHODS: The study lasted for 35 days. Twenty-four rats were divided into 4 groups: the control, with sodium fluoride (NaF) in the diet, with sodium fluoride, methionine and vitamin E (NaF+M+E) in the diet, with sodium fluoride and vitamin E (NaF+E) in the diet. The biochemical analysis conducted in animal liver homogenates included determination of activities of: total superoxide dismutase (t-SOD), superoxide dismutase with copper and zinc (CuZnSOD), superoxide dismutase with manganese (MnSOD), glutathione peroxidase (GPX), catalase (CAT), glutathione reductase (GR), glutathione S-transferase (GST) and the malondialdehyde (MDA) concentration. RESULTS: The activities of CuZn- SOD, GPX, CAT and MDA concentration were changed significantly. There were no differences in the activities of t-SOD, MnSOD, GR and GST among the experiment. CONCLUSIONS: In the conducted experiment, the run-out of enzymatic protection of liver by decreasing of the activities of antioxidant enzymes (CAT and GPX) and increasing the MDA concentration in NaF group was observed. The addition of vitamin E and methionine does not significantly stimulate the enzymatic antioxidant system, however, it causes of MDA concentration decreases. Med Pr 2018;69(4):403­412

Oxidative stress and angiogenesis in primary hyperparathyroidism.

BACKGROUND: The inappropriate elevation of parathormone (PTH), which regulates the process of angiogenesis in parathyroid tissue, causes the changes of activity of enzymes responsible for the removal of free radicals. Parathyroidectomy (PTX) in patients with primary hyperparathyroidism (PHPT) lowers the level of PTH and leads to the reduction of risk of cardiovascular and all-cause mortality by normalization of the antioxidant status. Therefore, the aims of the study were to assess the activity of antioxidant enzymes and free radical reaction products in patients after parathyroidectomy, and to evaluate the correlation between the systemic oxidative stress and angiogenic parameters. MATERIALS AND METHODS: Patients with PHPT treated surgically were enrolled into the study. Total antioxidant capacity (TAC), total oxidative status (TOS), oxidative stress index (OSI), superoxide dismutase (SOD), ceruloplasmin (CER), lipid hydroperoxides (LHP) and malondialdehyde (MDA) were measured before and after parathyroidectomy. The immunohistological expression of angiogenic factors in parathyroid specimens was assessed by the BrightVision method from ImmunoLogic using murine monoclonal anti-human: anti-VEGF, anti-CD31 and anti-CD106 antibodies. RESULTS: The significant increase of TAC, CER, reduction of TOS, MDA, SOD, especially for cytoplasmic form, and significant decrease of OSI, LHP were observed after PTX. There was no significant correlation between changes of oxidative stress markers and angiogenic parameters: VEGF, CD-31, CD-106 in parathyroid tissue. The correlation level was low and medium. CONCLUSIONS: Parathyroidectomy causes down-regulation of lipid peroxidation processes and leads to reduction of oxidative stress in patients with PHPT. The decrease in the OSI is the results of down-regulation of oxidative stress in the postoperative period. The change of the antioxidant status has no impact on angiogenesis processes in parathyroid tissue.

Influence of propofol on oxidative-antioxidative system parameters in peripheral organs of rats with Parkinson disease.

Propofol (2,6-diisopropylphenol) is a popular anaesthetic agent with antioxidant properties. The aim of the study was to assess the oxidant-antioxidant system parameters of particular organs (liver, kidney, heart, and lungs) in response to propofol administered to rats with Parkinson's disease and to healthy ones. The experiment was performed using 32 Wistar rats divided into four groups (8 rats each). The groups were as follows: 1 control, 2 Parkinson's disease, 3 control with propofol, 4 Parkinson's disease with propofol. Propofol was administered at a dose of 60 mg/kg body weight/IP, 60 minutes before decapitation. Animals were sacrificed and livers, kidneys, hearts and lungs were obtained for further biochemical analyses. The concentration of malondialdehyde (MDA), glutathione reductase (GR) activity, glutathione peroxidase (GPx) activity, glutathione S-transferase (GST) activity and catalase (CAT) activity were determined. In group 4 compared to group 2 there was observed a significant decrease in the MDA level in liver (71%), kidneys (51%) and heart (12%), increased GR activity in lungs (48%) and heart (34%), and increased CAT activity in liver (104%). In group 3 compared to group 1 there was a significant decrease in MDA level in kidneys (67%) and lungs (14%) and increased GR activity in heart (31%), liver (29%) and lungs (21%). Propofol can prevent or reduce damage caused by reactive oxygen species (ROS) by stimulating activity of antioxidative enzymes and inhibiting lipid peroxidation. Additionally, the response of tissues to administered propofol is different in Parkinson's disease and in healthy individuals.