The influence of occupational chronic lead exposure on the levels of selected pro-inflammatory cytokines and angiogenic factors.

The aim of the study was to determine the effect of occupational exposure to lead on the blood levels of pro-inflammatory cytokines and selected factors that influence angiogenesis. The study population was divided into two groups. The first group consisted of 56 male workers chronically exposed to lead. The second group (control) was comprised of 24 male administrative workers. The serum levels of interleukin 1ß (IL-1ß), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α) were significantly higher in the group of workers chronically exposed to lead compared to control values by 38%, 68%, and 57%, respectively. Similarly, the values of soluble vascular endothelial growth factor receptor-1 (sVEGFR-1) and fibroblast growth factor-basic (FGF-basic) were higher by 19% and 63%, respectively. In the group of workers chronically exposed to lead, there were positive correlations between the levels of pro-inflammatory cytokines (IL-1ß, IL-6, and TNF-α) and angiogenic factors (VEGF, FGF-basic, sVEGFR-1, and soluble angiopoietin receptor). In the control group, there were no correlations between the levels of the abovementioned parameters. Results of the present study indicate that chronic occupational lead exposure promotes inflammatory processes via induction of pro-inflammatory cytokines, modulates angiogenesis, and elicits interdependencies between the immune response and angiogenic factors.

Oxidative stress and motility impairment in the semen of fertile males.

The aim of the study was to determine the total oxidant status (TOS) and evaluate the influence of oxidative stress on sperm quality in fertile males. The study population consisted of 55 fertile males. Based on the seminal plasma TOS value, the study subjects were divided into the two subgroups: a group with a low (TOS-L) and a high (TOS-H) value. Comparing the TOS-H group with the TOS-L group, we found poorer sperm motility in the TOS-H group. We found lower total antioxidant capacity values and lower activity levels in the majority of the determined superoxide dismutase, glutathione peroxidase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase. Further, we found higher levels of copper and iron as well as lower levels of zinc in the TOS-H group. We observed lower medians of IL-2, 4, 6, 8 and INF-γ in the TOS-H group compared with the TOS-L group, whereas the medians of IL-1ß, IL-10 and IL-12 were significantly higher. In fertile males, higher oxidative stress intensity was associated with poorer semen quality and decreased antioxidant capacity in semen. These negative effects might be a result of decreased activities of antioxidant enzymes and altered levels of trace metals and cytokines.

The influence of chronic and subacute exposure to lead on the levels of prolactin, leptin, osteopontin, and follistatin in humans.

This study was designed to determine the levels of prolactin, leptin, osteopontin, and follistatin in workers chronically and subacutely exposed to lead compounds. The examined population consisted of three groups. The first group was composed of 56 male workers who were chronically exposed to lead for 13.38 ± 10.38 years. The second group served as a control group and consisted of 24 male administrative workers, while the third group included 32 male workers exposed to lead for 40 ± 3 days. The levels of leptin, osteopontin, and prolactin were significantly lower in the group of workers chronically exposed to lead than in the control group by 42%, 26%, and 41%, respectively. The levels of follistatin did not differ between those groups. The levels of all measured hormones did not change after a short-term exposure to lead compared to baseline. Chronic lead exposure is associated with significantly decreased level of prolactin, leptin, and osteopontin. Lead-induced changes in the levels of these hormones may disturb many functions of the human body, including the immune response, metabolism, reproduction, and bone turnover.

Oxidative DNA damage and oxidative stress in lead-exposed workers.

There are many discrepancies among the results of studies on the genotoxicity of lead. The aim of the study was to explore lead-induced DNA damage, including oxidative damage, in relation to oxidative stress intensity parameters and the antioxidant defense system in human leukocytes. The study population consisted of 100 male workers exposed to lead. According to the blood lead (PbB) levels, they were divided into the following three subgroups: a group with PbB of 20-35 µg/dL (low exposure to lead (LE) group), a group with a PbB of 35-50 µg/dL (medium exposure to lead (ME) group), and a group with a PbB of >50 µg/dL (high exposure to lead (HE) group). The control group consisted of 42 healthy males environmentally exposed to lead (PbB < 10 µg/dL). A comet assay was used to measure the DNA damage in leukocytes. We measured the activity of superoxide dismutase (SOD), catalase, glutathione reductase (GR), glucose-6-phosphate dehydrogenase (G6PD), and glutathione-S-transferase (GST) as well as the concentration of malondialdehyde (MDA), and the value of the total antioxidant capacity. The level of PbB was significantly higher in the examined subgroups than in the control group. The percentage of DNA in the tail was significantly higher in the LE, ME, and HE subgroups than in the control group by 10% ( p = 0.001), 15% ( p < 0.001), and 20% ( p < 0.001), respectively. The activity of GR was significantly lower in the LE and ME subgroups than in the control group by 25% ( p = 0.007) and 17% ( p = 0.028), respectively. The activity of G6PD was significantly lower in the ME subgroup by 25% ( p = 0.022), whereas the activity of GST was significantly higher in the HE subgroup by 101% ( p = 0.001) than in the control group. Similarly, the activity of SOD was significantly higher in the LE and ME subgroups by 48% ( p = 0.026) and 34% ( p = 0.002), respectively. The concentration of MDA was significantly higher in the LE, ME, and HE subgroups than in the control group by 43% ( p = 0.016), 57% ( p < 0.001), and 108% ( p < 0.001), respectively. Occupational lead exposure induces DNA damage, including oxidative damage, in human leukocytes. The increase in DNA damage was accompanied by an elevated intensity of oxidative stress.

The analysis of QT interval and repolarization morphology of the heart in chronic exposure to lead.

There are no common recommendations regarding electrocardiographic monitoring in occupationally exposed workers. Therefore, the present study was designed to investigate whether exposure to lead results in an increase of selected electrocardiography (ECG) pathologies, such as QT interval prolongation and repolarization disorders, in occupationally exposed workers. The study group included 180 workers occupationally exposed to lead compounds. The exposed group was divided according to the median of the mean blood lead level (PbBmean) calculated based on a series of measurements performed during 5-year observation period (35 µg/dl) into two subgroups: low exposure (LE, PbBmean = 20.0-35.0 µg/dl) and high exposure (HE, PbBmean = 35.1-46.4 µg/dl). The control group consisted of 69 healthy workers without occupational exposure to lead. ECG evaluation included the analysis of heart rate (HR), QT interval and repolarization abnormalities. Mean QT interval was significantly greater in the exposed population than in the control group by 2%. In the HE group, mean QT interval was significantly greater than in the control group by 4% and significantly different from those noted in the LE group. Positive correlations between QT interval and lead exposure indices were also reported. Besides, there was a negative correlation between HR and blood lead level. Increased concentration of lead in the blood above 35 µg/dl is associated with the QT interval prolongation, which may trigger arrhythmias when combined with other abnormalities, such as long QT syndrome. Therefore, electrocardiographic evaluation should be a part of a routine monitoring of occupationally exposed populations.

Lipid peroxidation and antioxidant enzymes in synovial fluid of patients with primary and secondary osteoarthritis of the knee joint.

OBJECTIVE: Osteoarthritis of the knee (KOA) is a common, age-related, joint disorder associated with loss of articular cartilage, osteophyte formation, sub-chodral bone change and synovitis. Recent studies have shown that reactive oxygen species (ROS) may participate in the initiation and progression of KOA. This study examines potential changes in the activities of antioxidant enzymes (superoxide dismutase, both isoenzymes zinc-copper superoxide dismutase and manganese superoxide dismutase) and glutathione transformation enzymes (glutathione peroxidase, glutathione reductase and glutathione-S-transferase) in synovial fluid of KOA patients, and estimates their relationship to the degree of lipid peroxidation in synovial fluid evaluated by malondialdehyde concentration, synovial fluid viscosity, type and duration of KOA. DESIGN: Synovial fluid samples obtained by transdermal arthrocentesis from 41 patients with KOA (23 had primary KOA and 18 had secondary KOA) and 22 control subjects were analyzed. Activities of antioxidant enzymes were analysed with the use of kinetic method, MDA concentration was measured fluorometrically by the Ohkawa method, and synovial fluid viscosity was measured using a cone-late viscometer Brookfield DV-II+ and a test by Ropes. RESULTS: Patients with KOA had significantly increased activities of all enzymes when compared to the control subjects for both KOA subgroups. The synovial fluid viscosity was significantly decreased and the synovial fluid test by Ropes was abnormal in KOA patients, mainly in the secondary KOA subgroup. The activities of all antioxidant enzymes were significantly negatively correlated with synovial fluid viscosity and duration of KOA. CONCLUSIONS: Patients with KOA display abnormal antioxidant status of synovial fluid with increased activities of antioxidant enzymes and decreased synovial fluid viscosity. Furthermore, synovial fluid viscosity, and activity of GR can be used to distinguish the primary from the secondary type of KOA.

Metabolic and antioxidative changes in liver steatosis induced by high-fat, low-carbohydrate diet in rabbits.

Significantly decreased amounts of carbohydrates and increase of fat in diet (Atkins' diet, Jan Kwasniewski's diet) may interfere with liver metabolism because main source of liver energy are carbohydrates. Large amount of fatty acid in diet may induce overproduction of reactive oxygen species in mitochondria because of increased oxidation and may cause steatosis. The influence of high-fat, low-carbohydrate diet (contained 14 g% protein, 25 g% fat, 8 g% carbohydrate) and compared to usual habitual diet (13 g% protein, 3 g% fat, 28 g% carbohydrate) as a control on liver function was examined in adult male rabbits. Fodder and water was ad libitum. The experiment lasted 24 weeks. At the beginning and every six weeks rabbits were weighed and blood was taken. Plasma glucose and cholesterol concentration, activity of glutamate dehydrogenase, alanine and aspartate in plasma and liver did not change. Concentrations of triacylglycerols (TG) in plasma were lower in the study group. Activity of aldolase increased in plasma and in liver in the study group while activity of sorbite dehydrogenase decreased in plasma at the end of the experiment. Malondialdehyde (MDA) concentration increased in aorta with no changes in liver and erythrocytes. Activity of glutathione peroxidase increased in erythrocytes and liver while total SOD increased only in the liver. High-fat, low-carbohydrate diet despite the lack of growth of the body mass, modifies significantly the homeostasis of carbohydrates and antioxidants in liver and enhanced production of TG in this organ, resulting in its steatosis.

The changes of alpha-amylase activity in serum and different tissues of female rat during sex cycle--isoelectrofocusing studies of alpha-amylase.

BACKGROUND: It has been suggested that hormonal changes may influence alpha-amylase activity during sex cycle. The aim of this study was to evaluate these changes in serum and different tissues during sex cycle in female rats. MATERIAL AND METHODS: The animals were assigned to proestrus, estrus, and diestrus groups depending on vaginal smears. We measured the activities of alpha-amylase in the serum, liver, salivary glands, pancreas and ovary of female rats, serum level of calcium, rat luteinising hormone (rLH) and rat follicle stimulating hormone (rFSH). The serum and tissue amylases were also characterized by wide-range polyacrylamide gel isoelectrofocusing. RESULTS: Statistically significant changes of alpha-amylase activity were found only in the ovary. The activity of alpha-amylase raised from proestrus (mean 303 +/- 124 IU/g) through estrus (mean 157 +/- 123 IU/g) and declined in diestrus (mean 81.9 +/- 51.6 IU/g). There were no statistically significant changes in the serum, liver, salivary glands and pancreas. We found two isoenzymes of alpha-amylase: one peak of amylase, present in the serum, liver, salivary gland and ovary with the mean isoelectric point of ca 5.34 and another present in ovary and pancreas with mean isoelectric point of ca 8.32. The only tissue found to contain both isoamylases was the ovary. We did not find any correlation between serum calcium level and alpha-amylase activity in the serum and ovary. CONCLUSION: The pattern of changes of alpha-amylase activity does not depend on the type of isoamylase in the tissue, but probably on the tissue influenced by the sex cycle. The changes of alpha-amylase activity are not mediated by calcium, they seem to result primarily from the profile of sex hormones affecting directly the target tissues.

Origin of serum alpha-amylase isoenzymes from healthy adult rats.

In connection with common use of rats in experimental testing drug toxicity in the liver or pancreas, we checked the electrophoretic patterns of amylase isoenzymes extracted from the liver, pancreas, parotis and serum of healthy adult rats. Separation of isoenzymes was made by polyacrylamide gel electrophoresis. The results indicate the salivary glands and liver as sources of serum alpha-amylase.