Comparative Assessment of Essential and Toxic Metals in the Blood of Rheumatoid Arthritis Patients and Healthy Subjects

Abstract

The present study deals with the comparative evaluation of essential and toxic metals in rheumatoid arthritis and healthy donors. Blood samples collected from rheumatoid arthritis patients and healthy subjects were analysed for selected essential and toxic metals (Ca, Mg, Fe, Zn, Cu, Co, Mn, Cr, Cd and Pb). The samples were digested in nitric acid and perchloric acid mixture, followed by quantification of the metals using atomic absorption spectrometry. Mean levels of Ca, Mg, Fe and Zn were significantly higher in the blood of healthy donors; however, elevated levels of Cd, Co, Cr, Cu and Pb were observed in blood of the patients. The correlation coefficients among the selected metals in the blood of arthritis patients were significantly different compared with the healthy counterparts. Multivariate cluster analysis revealed mutual apportionment of the essential and toxic metals in blood of the patients, whereas, in controls, the essential and toxic metals revealed diverse apportionment. Variations in the metal levels with gender, residence and smoking habits were also evaluated in both donor groups. Relative distribution, correlation and apportionment of the essential and toxic metals in the blood of the patients were significantly different than of controls.

Clinical Correlations Between Cesium, Cobalt, Manganese, Rubidium and Rhenium with the Pathogenesis of Rheumatoid Arthritis

“…The result of the current study was consistent with the previous result [17] While, the result of current study was not agreeable was with previous results [18],who reported that the mean serum levels of cobalt was significantly lower than control group.…”

Association between serum trace element concentrations and the disease activity of systemic lupus erythematosus

“…Se is an essential constituent of anti-oxidative enzymes including selenoprotein P, glutathione peroxidases and thioredoxin reductases which are responsible for Se transport (selenoprotein P), antioxidant/redox properties (glutathione peroxidases (GPxs), thioredoxin reductases and selenoprotein P) and anti-inFammatory properties (selenoprotein S and GPx4). 8 Rheumatoid arthritis has previously been investigated with respect to the role of trace elements in disease activity, [9][10][11] and there are limited data available concerning lupus. 12 Because of the potential importance of trace elements in the pathogenesis of SLE, and especially the vital role of Zn, Cu and Se in oxidative defense, the current study was designed to evaluate the relationship between serum values of these trace elements and lupus disease activity in addition to disease manifestations.…”

“…Rheumatoid arthritis has previously been investigated with respect to the role of trace elements in disease activity, 9–11 and there are limited data available concerning lupus. 12 Because of the potential importance of trace elements in the pathogenesis of SLE, and especially the vital role of Zn, Cu and Se in oxidative defense, the current study was designed to evaluate the relationship between serum values of these trace elements and lupus disease activity in addition to disease manifestations.…”

Etiopathogenic mechanisms of tobacco constituents in rheumatoid arthritis

“…Chromium and cobalt ions (Cr 3+ and Co 2+ ) affect the macrophage-like cells. lead damages osteoblasts and chondrocytes also due to the oxidative stress (26). The cadmium from cigarette smoke reacts with previously inhaled fine particulate matter generated by the environmental pollution, generating cadmium oxide nanoparticles, which stimulates protein citrullination in lung epithelial cells, causing ra (11).…”

“…The cadmium from cigarette smoke reacts with previously inhaled fine particulate matter generated by the environmental pollution, generating cadmium oxide nanoparticles, which stimulates protein citrullination in lung epithelial cells, causing ra (11). Toxic metals, such as mercury, nickel, lead and arsenic induce oxidative stress by depleting glutathione and protein-bound sulfhydryl groups (26).…”