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.
The aim of this study was to estimate the activity of glutathione peroxidase (GPx), glutathione reductase (GR), and malondialdehyde (MDA) in erythrocytes in healthy male employees of zinc and lead steelworks who were occupationally exposed to lead over a long period of time (about 15 yr). Workers were divided into two subgroups: the first included employees with low exposure to lead (LL) (n=75) with blood lead level PbB=25-40 microg/dL and the second with high exposure to lead (HL) (n=62) with PbB over 40 microg/dL. Administration workers (n=35) with normal levels of PbB and zinc protoporphyrin in blood (ZPP) in blood were the control group. The activity of GPx significantly increased in LL when compared to the control group (p<0.001) and decreased when compared to the HL group (p=0.036). There were no significant changes in activity of GR in the study population. MDA erythrocyte concentration significantly increased in the HL group compared to the control (p=0.014) and to the LL group (p=0.024). For the people with low exposure to lead (PbB=25-40 microg/dL), the increase of activity of GPx by about 79% in erythrocytes prevented lipid peroxidation and it appears to be the adaptive mechanism against the toxic effect of lead. People with high exposure to lead (with PbB over 40 microg/dL) have shown an increase in MDA concentration in erythrocytes by about 91%, which seems to have resulted from reduced activity of GPx and the lack of increase in activity of GR in blood red cells.
(1) lead increases erythrocyte MDA concentration and the activity of GPx as well as SOD in normotensive subjects. (2) Among individuals exposed to lead, with arterial hypertension diagnosed, higher body mass index, age, values of blood lead level, and prolonged exposure to lead have been noticed, accompanied by intensified oxidative stress and the decrease in the activity of glutathione peroxidase in erythrocytes. The reasons for increase of blood pressure in lead exposure remain unrecognized.
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