Association between subchronic and chronic lead exposure and levels of antioxidants and chemokines.

PURPOSE: This study aimed to compare the influence of lead on the non-enzymatic antioxidant defenses and the levels of chemokines in workers subchronically and chronically exposed to lead. METHODS: The study population was divided into three groups. The first group consisted of male workers subchronically exposed to lead for 40 ± 3.2 days, while the second group included male workers chronically exposed to lead. The third group was a control group. RESULTS: The levels of uric acid and bilirubin were significantly higher after a subchronic exposure to lead compared to the baseline by 22 and 35 %, respectively. Similarly, the values of total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI) increased by 15, 50, and 33 %, respectively. At the same time, the levels of thiol groups and albumin decreased by 5 and 8 %, respectively. Additionally, the levels of interleukin-8 (IL-8) and macrophage inflammatory protein-1ß (MIP-1ß) were significantly higher after a subchronic exposure to lead compared to the baseline by 34 and 20 %, respectively. Moreover, IL-8 level was significantly higher by 40 % in the group of workers chronically exposed to lead than in the control group, while the level of interferon gamma-induced protein-10 (IP-10) was significantly lower by 28 %. CONCLUSIONS: Similar to chronic lead exposure, subchronic exposure to lead is associated with elevated blood levels of uric acid and bilirubin in humans. This probably results in increased TAC value despite thiol depletion. However, the compensatory activation of non-enzymatic antioxidant defenses seems to be insufficient to protect against lead-induced oxidative stress, which may be additively enhanced by the pro-inflammatory action of chemokines, especially IL-8.

Effects of Propofol on Oxidative Stress Parameters in Selected Parts of the Brain in a Rat Model of Parkinson Disease.

INTRODUCTION: Propofol is an intravenous sedative-hypnotic agent that is commonly used to induce and maintain general anaesthesia. This drug has antioxidant properties, which are partly caused by a phenolic structure similar to α-tocopherol. The present study aimed to evaluate the effect of propofol on the level of oxidative stress biomarkers in the frontal cortex, striatum, thalamus, hippocampus and cerebellum in rats with experimental Parkinson's disease (PD). MATERIAL/METHODS: The experiment was performed on 24 male Wistar rats assigned to the following groups: 1 - control; 2 - PD; 3 - PD with propofol. The dopaminergic systems were damaged with 6-hydroxydopamine (6-OHDA) administered to each lateral ventricle (2x15 µg/5 µl). 60 mg/kg of propofol was later given to the 8-week-old rats intraperitoneally. The activities of superoxide dismutase (SOD) and its enzymes Cu/ZnSOD and MnSOD, together with the malondialdehyde (MDA) concentration, total oxidative status (TOS) and total antioxidant capacity (TAC), were measured. RESULTS: In the 2nd group, a significant increase in MDA concentration in the striatum, hippocampus and thalamus, and an increase of TOS in the striatum, thalamus and cerebellum were noted, along with a TAC decrease in the cortex, striatum and thalamus. Propofol caused a significant decrease in MDA levels in the cortex, striatum, hippocampus and thalamus, and a decrease in TOS levels in the cortex, striatum and cerebellum, with increased TAC in all evaluated structures. CONCLUSIONS: A shortage of natural antioxidants is observed in PD, along with an increase in pro-oxidants in many brain areas. Propofol inhibits oxidative stress in the brain, which shows its neuroprotective properties against oxidative damage.

Activity of Antioxidant Enzymes in the Tumor and Adjacent Noncancerous Tissues of Non-Small-Cell Lung Cancer.

Lung tissue is directly exposed to high oxygen pressure, as well as increased endogenous and exogenous oxidative stress. Reactive oxygen species (ROS) generated in these conditions play an important role in the initiation and promotion of neoplastic growth. In response to oxidative stress, the antioxidant activity increases and minimizes ROS-induced injury in experimental systems. The aim of the present study was to evaluate the activity of antioxidant enzymes, such as superoxide dismutase (SOD; isoforms: Cu/ZnSOD and MnSOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione S-transferase (GST), along with the concentration of malondialdehyde (MDA) in tumor and adjacent noncancerous tissues of two histological types of NSCLC, i.e., adenocarcinoma and squamous cell carcinoma, collected from 53 individuals with surgically resectable NSCLC. MDA concentration was similar in tumors compared with adjacent noncancerous tissues. Tumor cells had low MnSOD activity, usually low Cu/ZnSOD activity, and almost always low catalase activity compared with those of the corresponding tumor-free lung tissues. Activities of GSH-related enzymes were significantly higher in tumor tissues, irrespective of the histological type of cancer. This pattern of antioxidant enzymes activity could possibly be the way by which tumor cells protect themselves against increased oxidative stress.

Antioxidant Enzyme Activities in Rabbits Under Oxidative Stress Induced By High Fat Diet.

INTRODUCTION: The aim of this study was to investigate whether the type and form of oil (raw/non-oxidised (N) or post-frying/oxidised (O)) consumed in high-fat diets affect the oxidative status of an organism, as observed by malondialdehyde (MDA) concentration as an oxidative factor and antioxidant enzyme activity. MATERIAL AND METHODS: Fats in the diet came from rapeseed oil (R) and olive oil (O). RESULTS: The applied diet caused a decrease in MDA concentration (µmol/L) in serum in group RN from 2.94 ± 0.87 to 1.76 ± 0.13, in group ON from 2.45 ± 0.62 to 1.50 ± 0.10, and in group OO from 2.70 ± 1.16 to 1.84 ± 0.36. Meanwhile, MDA concentration (mmol/L) increased in blood haemolysate in group RO from 0.15 ± 0.07 to 0.22 ± 0.03 and in group OO from 0.17 ± 0.02 to 0.22 ± 0.02. The observed changes caused a response of the enzymatic antioxidant system in both models, especially followed by an increase in activities of total superoxide dismutase and its mitochondrial isoenzyme in all experimental groups, while its cytosolic isoenzyme activity increased only in ON and OO groups. Increased activity of glutathione peroxidase (GPX) in groups RN and RO and of catalase (CAT) in groups ON and OO was observed. Significant differences in responses to the different types and forms of oils were probably caused by the different oxidative stability of the studied oils. CONCLUSION: This diet disturbed the body's oxidative status; however, during the six-month study the enzymatic antioxidant system remained effective.

The Effect of a Short-Term Exposure to Lead on the Levels of Essential Metal Ions, Selected Proteins Related to Them, and Oxidative Stress Parameters in Humans.

The present study was designed to explore the possible influence of subacute exposure to lead on the levels of selected essential metals, selected proteins related to them, and oxidative stress parameters in occupationally exposed workers. The study population included 36 males occupationally exposed to lead for 36 to 44 days. Their blood lead level at the beginning of the study was 10.7 ± 7.67 µg/dl and increased to the level of 49.1 ± 14.1 µg/dl at the end of the study. The levels of calcium, magnesium, and zinc increased significantly after lead exposure compared to baseline by 3%, 3%, and 8%, respectively, while the level of copper decreased significantly by 7%. The malondialdehyde (MDA) level and the activities of catalase (CAT) and superoxide dismutase (SOD) did not change due to lead exposure. However, the level of lipid hydroperoxides (LPH) in serum increased significantly by 46%, while the level of erythrocyte lipofuscin (LPS) decreased by 13%. The serum levels of essential metals are modified by a short-term exposure to lead in occupationally exposed workers. A short-term exposure to lead induces oxidative stress associated with elevated levels of LPH but not MDA.

Effects of Propofol on the Liver Oxidative-Antioxidant Balance in a Rat Model of Parkinson's Disease.

BACKGROUND: Parkinson's disease is caused by the destruction of dopaminergic neurons in the substantia nigra of the midbrain. One of the possible factors involved in the pathogenesis of Parkinson's disease is impaired oxidativeantioxidative balance. OBJECTIVES: The present study aimed to evaluate selected parameters of the liver oxidative-antioxidative system in a Wistar rat model with Parkinson's disease treated with propofol. MATERIAL AND METHODS: Experiments were performed on 32 rats divided into 4 groups: 1 - control, 2 - Parkinson's disease, 3 - control with propofol, 4 - Parkinson's disease with propofol. The rats were decapitated at 8 weeks of age and their livers were collected. In the liver, the activities of catalase (CAT), glutathione peroxidase (GPx), glutathione transferase (GST), glutathione reductase (GR) and the concentrations of: Malondialdehyde (MDA), total antioxidant capacity (TAC), total oxidant status (TOS) were assessed. RESULTS: The study demonstrated a decrease in CAT activity and an increase in MDA, TOS concentrations in group 2 compared to that of group 1. Administration of propofol in rats of group 4 caused an increase in CAT activity and a decrease in MDA concentration compared to that of group 2 and an increase in TAC, CAT, GR levels, decrease in MDA levels compared to that of group 1. There was also an increase in GR and TAC in group 3 compared to that of group 1. CONCLUSIONS: Propofol in Parkinson's disease stimulates the production of antioxidant enzymes in the liver, simultaneously decreasing oxidative stress, which has a beneficial effect on the oxidative-antioxidative balance.