Thiol-disulfide homeostasis and ischemia-modified albumin levels as indicators of oxidative stress in welders' lung disease.

Welders' lung disease refers to mixed exposure to different kinds of metals and chemicals from welding fumes, which affect all parts of the respiratory tract including airways and parenchyma together. This study aimed to investigate the oxidative status in patients with welders' lung (PWL) by means of thiol-disulfide homeostasis and ischemia-modified albumin (IMA) levels. The male welder workers diagnosed with welders' lung disease and healthy individuals were recruited in the study. Plasma levels of disulfide, disulfide/native thiol ratio, disulfide/total thiol ratio, IMA, and catalase (CAT) were determined. Pulmonary function test parameters of both groups were compared. The thiol-disulfide homeostasis parameters of PWL and control group were as follows: disulfide (20.5 ± 6.3 vs. 16.2 ± 3.9 µmol L-1, p < 0.001), disulfide/native thiol (4.36 (1.59) vs. 4.0 (1.64), p = 0.024), and disulfide/total thiol (4.01 (1.34) vs. 3.71 (1.41), p = 0.024). IMA levels in PWL were significantly higher than the control group (1.37 (0.27) mg dL-1 vs. 0.49 (0.61) mg dL-1, p < 0.001), whereas CAT activities were significantly higher in the control group (106.6 (54.5) kU L-1 vs. 78.3 (67.8) kU L-1, p = 0.003). The findings of the present study revealed that oxidative stress plays a key role in the pathogenesis of welders' lung disease. Plasma thiol-disulfide homeostasis and IMA levels might be indicators of oxidative stress in PWL.

The compromise of dynamic disulfide/thiol homeostasis as a biomarker of oxidative stress in trichloroethylene exposure.

In this study, we aimed to investigate disulfide/thiol homeostasis in trichloroethylene (TCE) exposure. The study was carried out in 30 nonsmoker TCE-exposed workers with a variety of occupations. Additionally, 30 healthy nonsmoker volunteers were recruited as the control group. TCE exposure was determined by measuring urinary trichloroacetic acid (TCA) concentration. Median urinary TCA levels of exposed workers (20.5 mg/L) were significantly higher than control subjects (5 mg/L). Thiol and disulfide concentrations were determined using a novel automated method. Disulfide/thiol ratio was significantly higher in the exposed group (p < 0.001). Thiol/disulfide homeostasis was found to be disturbed in TCE-exposed workers. We predict that in TCE-exposed workers this disturbance can be a therapeutic target, and the efficiency of the treatment can easily be monitored by the novel method we used.