BackgroundManganese (Mn) is widely used in industries including the manufacture of Mn-iron (Fe) alloy. Occupational Mn overexposure causes manganism. Mn is known to affect Fe metabolism; this study was designed to test the hypothesis that workers exposed to Mn may have an altered expression of mRNAs encoding proteins in Fe metabolism.MethodsWorkers occupationally exposed to Mn (n= 71) from a Mn–Fe alloy factory and control workers without Mn-exposure (n= 48) from a pig-iron plant from Zunyi, China, were recruited for this study. Blood samples were collected into Trizol-containing tubes. Total RNA was isolated, purified, and subjected to real-time RT-PCR analysis. Metal concentrations were quantified by atomic absorption spectrophotometry.ResultsWorking environment and genetic background of both groups were similar except for marked differences in airborne Mn concentrations (0.18 mg/m3in Mn–Fe alloy factory vs. 0.0022 mg/m3in pig-Fe plant), and in blood Mn levels (34.3 µg/L vs. 10.4 µg/L). Mn exposure caused a significant decrease in the expression of divalent metal transporter-1 (DMT1), transferrin (Tf) and hepcidin by 58.2%, 68.5% and 61.5%, respectively, as compared to controls, while the expression of transferrin receptor (TfR) was unaltered. Linear regression analysis revealed that expressions of DMT1, Tf and hepcidin were inversely correlated with the accumulative Mn exposure; the correlation coefficients (r) are −0.47, −0.54, and −0.49, respectively (p< 0.01).ConclusionThe data suggest that occupational Mn exposure causes decreased expressions of DMT1, Tf and hepcidin in blood cells; the finding will help understand the mechanism underlying Mn exposure-associated alteration in Fe homeostasis among workers.
Cross-sectional study of expression of divalent metal transporter-1, transferrin, and hepcidin in blood of smelters who are occupationally exposed to manganese