The Effect of Occupational Exposure to Lead on the Non-Enzymatic Antioxidant System

Abstract

Background: The role of non-enzymatic antioxidants, such as uric acid, albumin, bilirubin, and α-tocopherol, in lead poisoning remains unclear. Therefore, the aim of the study was to explore the association between occupational exposure to lead and nonenzymatic antioxidant concentrations in serum and plasma. Material and Methods: The study population consisted of 278 healthy male employees of lead-zinc plants, with 129 workers classified as having low lead exposure (blood lead level -PbB = 20-39.9 μg/dl) and 149 workers classified as having high lead exposure (PbB = 40-59.8 μg/dl). The control group was composed of 73 healthy male administrative workers. No one from this group had blood lead level or zinc protoporphyrin (ZPP) level greater than normal levels, being 10 μg/dl and 2.5 μg/g of hemoglobin, respectively. In addition to the levels of PbB and ZPP, serum levels of uric acid (UA), albumin, thiol groups of albumin, and bilirubin were determined. The ferric reducing ability of plasma (FRAP) and the plasma level of α-tocopherol were also evaluated. Results: Lead exposure indices were significantly elevated in the examined subgroups as compared with the controls. Serum uric acid levels were significantly elevated in both subgroups, particularly in the group with high exposure. Serum bilirubin concentration was significantly elevated in the group with high exposure compared with the control group, while in the group with low exposure, it showed only a non-significant trend towards an increase. In contrast, ferric-reducing ability of plasma was not significantly greater in the examined subgroups as compared with the control group. Nevertheless, levels of albumin, thiol groups of albumin, and α-tocopherol levels were significantly decreased in the exposed subgroups compared with the control group. Conclusions: Occupational exposure to lead interferes with the blood non-enzymatic antioxidant system. Med Pr 2014;65(4): [443][444][445][446][447][448][449][450][451]

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

“…The negative results of these studies may be due to the complexity of the possible interactions between lead and heme metabolism. On the one hand, it is well documented that lead inhibits heme biosynthesis (Dobrakowski et al 2014). Consequently, the depletion of the heme pool may result in its decreased degradation and less bilirubin synthesis.…”

“…Because of their ROS scavenging activity, thiol groups of cysteine residues of albumin determine the plasma redox status (Dobrakowski et al 2014). Therefore, decreased level of thiol groups, observed in the present study may be secondary to the decrease in albumin level.…”

“…Therefore, decreased level of thiol groups, observed in the present study may be secondary to the decrease in albumin level. The second possible explanation for the reduced thiol group level is the well-documented high affinity of lead toward thiol groups (Dobrakowski et al 2014). In accordance with the human studies, decreased level of thiol groups was also reported in experimental studies in rats (El-Missiry 2000; Tandon et al 2002).…”

“…In our previous study, we reported higher levels of uric acid in workers chronically exposed to lead compounds (Blood lead (PbB) = 40.40 ± 10.05 µg/dl) for, on average, 16.40 ± 10.20 years compared to the unexposed control group (PbB = 6.39 ± 2.47 µg/dl). Besides, we reported increased levels of other non-enzymatic antioxidants, such as bilirubin, albumin, thiol groups, and α-tocopherol (Dobrakowski et al 2014). However, the possible association between lead toxicity and the non-enzymatic antioxidant defenses is not fully understood and needs further investigation.…”

“…Besides, lead is able to dysregulate the antioxidant defenses, including the antioxidant enzymes and the non-enzymatic antioxidants, such as uric acid. (Dobrakowski et al 2014; Soliman et al 2015; Wang et al 2012). In our previous study, we reported higher levels of uric acid in workers chronically exposed to lead compounds (Blood lead (PbB) = 40.40 ± 10.05 µg/dl) for, on average, 16.40 ± 10.20 years compared to the unexposed control group (PbB = 6.39 ± 2.47 µg/dl).…”