Dynamic thiol disulfide homeostasis in painters as indices of oxidative stress.

This study was designed to determine thiol-disulfide homeostasis as indices of oxidative stress in painters by using a novel and automated colorimetric measurement method. Male painters (n = 117) were separated into three groups according to duration of work; group 1 (<5 years), group 2 (5-14 years) and group 3 (≥15 years). Hippuric acid, trichloroacetic acid (TCA), and phenol in urine was determined. Catalase activity and ischemia-modified albumin (IMA) levels were also assessed. Disulfide/Native Thiol and Disulfide/Total Thiol of group 2 and group 3 were significantly higher than those of group 1 (p < 0.001). A positive correlation was observed between urinary phenol and disulfide/native thiol (r = 0.214, p = 0.035), IMA (r = 0.305, p = 0.002), disulfide (r = 0.209, p = 0.040), and duration of work (r = 0.341, p < 0.001). The newly developed automated colorimetric method used in our study proposes a promising, practical and daily applicable test for evaluating oxidative status of painters.

Assessment of Diastolic Function and Thiol-Disulphide Homeostasis in Arsenic-Exposed Workers.

OBJECTIVES: Exposure to arsenic is associated with various cardiovascular diseases. The imbalance between antioxidant and oxidant homeostasis plays a crucial role in the cardiovascular effects of arsenic. The aim of this study was to investigate the effect of arsenic exposure on diastolic function by measuring thiol and disulphide in arsenic-exposed workers. METHODS AND RESULTS: A total of 107 male arsenic-exposed workers and 36 healthy subjects were enrolled. Mitral inflow velocity and parameters of diastolic function were measured. As oxidative stress indicators, total thiol, native thiol, disulphide, and their percent ratios were determined. The mean age was 39.1 ± 9.5 years in the arsenic-exposed group and 37.4 ± 9.6 years in the controls. The median blood arsenic level was 42 µg/dL in the arsenic-exposed group and 3.75 µg/dL in the controls. E-wave, E/A ratio, and e' wave were lower and left atrial diameter, A-wave, average E/e' ratio, and tricuspid regurgitation velocity were higher in the arsenic-exposed group. Native and total thiol concentrations were lower, and disulphide/native and disulphide/total thiol ratios were higher in the arsenic-exposed group. Fourteen (13.1%) workers had diastolic dysfunction, 26 (24.3%) had indeterminate, and 67 (62.6%) had normal diastolic function, compared to 1 (2.8%), 2 (5.6%), and 33 (97.7%) in the control group, respectively. In regression analysis, disulphide/native thiol ratio (p < 0.001) and blood arsenic level (p < 0.001) predicted increased average E/e' ratio in the arsenic-exposed group. CONCLUSIONS: This study showed strong associations among arsenic exposure, oxidative stress, and diastolic function, and revealed the influence of arsenic exposure on diastolic dysfunction through oxidative stress.

Alteration of thiol disulfide homeostasis and ischemia-modified albumin levels as indicators of oxidative status in patients with silicosis.

The aim of this study was to evaluate the oxidative status in patients with silicosis by detecting dynamic thiol disulfide homeostasis (TDH), ischemia-modified albumin level (IMA) catalase (CAT) activity, and the correlation of these markers with pulmonary function tests. Male ceramic workers with silicosis (n = 91) and healthy individuals (n = 47) were recruited for the study. Radiographic abnormalities of pneumoconiosis were classified into three profusion categories (categories 1, 2, and 3), and patients with silicosis, those with category 1, were defined as group 1 and those with category 2 or 3 were defined as group 2. Plasma levels of native thiol (NT), total thiol (TT), disulfide (Ds), IMA, and CAT activities were determined. Pulmonary function tests of groups were compared. NT, TT, and NT/TT ratios were significantly lower in groups 1 and 2 than the control group (p < 0.05). These did not differ between patients with silicosis (groups 1 and 2) and control group (p = 0.421). Ds/NT and Ds/TT ratios were significantly higher in group 2 than the control group (p < 0.05). NT, TT, and Ds did not differ significantly between groups 1 and 2. The oxidant biomarker IMA was higher (p < 0.001), and the antioxidant parameters albumin and CAT were lower in groups 1 and 2 (p < 0.001) compared with the control group. The mean FEV1act, FVCact, forced expiratory volume in 1 second/forced vital capacity (%), and value of 25-75 percent maximum expiratory flow were significantly lower in groups 1 and 2 than control group. We have used a novel colorimetric method to assess TDH in patients with silicosis. Alteration of plasma thiol/disulfide homeostasis and IMA levels might be novel indicators of oxidative stress in silicosis.

Neutrophil-to-Lymphocyte Ratio and Platelet-to-Lymphocyte Ratio as Inflammatory Markers in Patients With Welders' Lung Disease.

OBJECTIVE: To investigate neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) in patients with welders' lung disease (PWLD) and its relation with pulmonary function parameters. METHODS: One hundred sixteen male PWLD and 118 healthy non-exposed individuals were recruited. Pulmonary function tests (PFTs), complete blood count, erythrocyte sedimentation rate (SED), c-reactive protein (CRP), NLR and PLR of both groups were retrospectively analyzed. RESULTS: NLR, PLR, WBC, ESR, and CRP were significantly higher in PWLD compared to controls (all P < 0.001). All PFTs, except for FEV1/FVC, significantly decreased in PWLD compared to controls as. NLR correlated positively with ESR (r = 0.241 and P < 0.001). CONCLUSION: Our results show that NLR and PLR can be considered as new inflammatory markers in PWLD with their cheap, fast and easily measurable feature with routine blood count analysis.

Dynamic thiol/disulphide homeostasis as indicator of oxidative stress in automotive workers.

Purpose: To examine thiol-disulphide homeostasis auto painters.Materials and methods: A total of 115 male workers, including 60 auto painters workers and 55 reference group, of the painting and assembly line units respectively, were included in the study. Thiol-disulphide parameters and ischaemia-modified albumin (IMA) of groups were determined. Urinary hippuric acid, (HA) phenol, hexanedione, trichloroacetic acid, arsenic and blood lead and manganese were analysed.Results: The median urinary HA level was significantly higher in auto painters when compared to the reference group [(2461 (1212) vs. 520 (513) µgr/L), (p < 0.001)] . The mean disulphide level [19.7 (4.3) vs 0.15.1(4.1) µmol/L, (p < 0.001)], the disulphide/native thiol ratio [4.72 (1.47) vs. 3.13 (1.21, (p < 0.001)] and the disulphide/total thiol ratio [4.31 (1.23) vs. 2.94 (1.06), (p < 0.001)] were higher in auto painters when compared to the reference group. There was a statistically significant positive correlation between urinary HA and disulphide concentrations (r = 0.536 and p < 0.001), disulphide/native thiol ratio (r = 0.564 and p < 0.001) and the disulphide/total thiol ratio (r = 0.564 and p < 0.001) and IMA (r = 0.396 and p < 0.001).Conclusion: The results presented in this study showed that oxidative stress can be associated with occupational exposure to toluene denoted by alteration of thiol disulphide homeostasis and ischaemia-modified albumin levels.

Radiological progression and lung function decrements among silica-exposed ceramic workers: a longitudinal study.

Objectives: This follow-up study set out to evaluate the natural course and radiographic progression of silicosis among ceramic workers and describe the risk factors related with disease progression. Materials and methods: We retrospectively analyzed the data of ceramic workers with silicosis who were referred to our hospital between February 2010 and March 2018. A total of 165 ceramic workers followed at least 24 months and with at least two chest radiographs were included in the study. Results: The duration of silica exposure ranged from 5.5 to 27 (median 13.6) years. The numbers of patients according to follow-up time were as follows: 38 (2-2.9) years, 77 (3-3.9) years, 26 (4-4.9) years, 17 (5-5.9) years, and 7 (≥6) years. Overall 62 of 165 (37.5%) cases showed radiologic evidences of progression ranging from 2 to 8.9 years (mean 3.7 years). Pulmonary function loss rate among silicosis patients was 36.9% (61/165). Multiple logistic regression analysis showed a significant relation between radiographic progression and age (OR, 1.079: 95% CI, 1.011-1.152), follow-up time (OR, 1.557: 95% CI, 1.144-2.118), and the ILO category (category 2 or 3) at first visit (OR, 3.507: 95% CI, 1.505-8.170). Conclusions: Our findings suggest that one-third of Turkish ceramic workers with silicosis who were followed up to 8.9 years showed progression that was related to increasing age greater ILO category at time of initial visit and follow-up duration.

Serum endocan level and diastolic functions in the case of lead exposure

Background/aim: Lead can cause morphological and functional changes in heart, and inflammation and endothelial dysfunction in vasculature. Endocan, as a novel indicator of endothelial dysfunction, has been used for cardiovascular diseases. This study investigated the relationship between lead exposure, endocan levels, and diastolic functions. Materials and methods: A total of 51 lead-exposed workers without a known cardiovascular disease or risk factors and 54 healthy controls were enrolled. All participants underwent transthoracic echocardiography. Blood lead and serum endocan levels were analyzed. Results: Baseline demographic and clinical characteristics were found to be similar between groups. Median blood lead (32 vs 1.5 µg/dL, P < 0.001) and serum endocan levels (67 vs 57.1 pg/mL, P = 0.02) were significantly higher in the lead-exposed group. Serum endocan level showed a positive correlation with blood lead levels (r = 0.404, P = 0.003) in lead-exposed workers. Serum endocan level was an independent risk factor for increased E/E' ratio (ß = 0.704, P = 0.002) and left atrial volume index (ß = 1.158, P = 0.011) and higher level of lead in blood was an independent risk factor for increased E wave (ß = 8.004, P = 0.022) in lead-exposed workers. Conclusion: Worsened diastolic functions may be seen in the course of lead exposure. Due to sharing a similar mechanism, a higher serum level of endocan may be a valuable laboratory clue for impaired diastolic function in this population.

A new potential biomarker in early diagnosis of firefighter lung function impairment: dynamic thiol/disulphide homeostasis.

OBJECTIVES: The aim of this study was to investigate the associations between urinary arsenic, oxidative stress, assessed by thiol/disulphide homeostasis, and lung diseases in firefighters. METHODS: The study conducted among the municipality-based male firefighters (n = 100) who were admitted to occupational diseases clinic for periodic medical examination. The control group consisted of non-exposed male office workers (n = 50). Urinary arsenic levels, thiol/disulphide homeostasis parameters of participants were determined. Also, lung diseases were assessed by chest X-ray and pulmonary function tests. RESULTS: The mean age and work year did not differ in the study and control group. The median urinary arsenic concentration of firefighters was significantly higher than in the control group: 15.65 (2.5-246) µg/L and 3 (0.10-6) µg/L, respectively (p < 0.001). The parameters of pulmonary function tests (PFT) FVC (%), FEV1 (%), FEV1/FVC ratio and FEF 25-75 (%) were all significantly lower in firefighters compared to controls. A significant increase in mean serum disulphide concentration (17.10 ± 8.31 µmol/L vs. 7.48 ± 5.91) (Fig. 1) and disulphide/native thiol % ratio: 3.63 (0.53-11.43) vs. 1.51 (0.03-7.65) (p < 0.001) were found between exposed group and controls. The Spearman's correlation analysis revealed a positive correlation between urinary arsenic and disulphide (r = 0.422, p < 0.001), disulphide/native thiol % ratio (r = 0.409, p < 0.001). Nevertheless, urinary arsenic correlated negatively with all PFT parameters including FVC (%), FEV1 (%), FEV1/FVC and FEF 25-75 (%) (p < 0.001). CONCLUSION: We showed the arsenic-induced oxidative stress in firefighters with impairments of several lung functions determined by thiol/disulphide homeostasis using a novel method.

Occupational exposure to asphalt fume can cause oxidative DNA damage among road paving workers.

OBJECTIVES: We designed the present study to determine the effect of occupational exposure to asphalt fumes on oxidative status and DNA damage in road paving workers. METHODS: Sixty road paving workers exposed to asphalt fumes and forty non-exposed control subjects were recruited. Occupational exposure to PAHs was assessed by urinary 1-hydroxypyrene (1-OHP) excretion. Serum thiol disulfide homeostasis (TDH), total oxidant status (TOS) and total antioxidant status (TAS) and urinary 8-hydro-deoxyguanosine (8-OH-dG) level were evaluated by automated colourimetric method. RESULTS: The urinary concentrations of 1-OHP and 8-OH-dG were significantly higher in the exposed group than in the control group (P < 0.001). Disulfide/thiol ratio, TOS, and TAS were also significantly higher for the asphalt workers. A positive correlation existed between urinary 1-OHP and 8-OH-dG, TOS and TAS. CONCLUSION: Study results indicate that exposure to PAHs induces oxidative stress and causes genotoxic effects in asphalt workers.

Alteration of thiol-disulfide homeostasis in workers occupationally exposed to arsenic.

This study evaluates the redox state in occupationally arsenic-exposed workers (n = 71) by assessing the dynamic serum thiol-disulfide homeostasis. We determined the serum thiol-disulfide homeostasis parameters of exposed workers and controls (n = 43) using a novel automated colorimetric assay. Median urinary As and 8-isoprostane levels of exposed group were significantly higher than control group (16.40 µg/L vs 2µg/L, p < .001 and 2.28 ng/ml vs 0.54 ng/ml, p < .001, respectively). Disulfide level, disulfide/native thiol ratio, and disulfide/total thiol ratio were significantly higher in exposed group. The mean ceruloplasmine and myeloperoxidase activities of As-exposed group were significantly higher than control group (117.15 U/L vs 87.02 U/L, p = .035 and 148.53 U/L vs 97.75 U/L, p = .000, respectively). The median catalase activity did not differ in the two groups. Our findings revealed that As disrupts the thiol-disulfide homeostasis in favor of disulfide.

Evaluation of Dynamic Disulphide/Thiol Homeostasis in Silica Exposed Workers.

BACKGROUND: Oxidative stress is implicated as one of the main molecular mechanism underlying silicosis. AIMS: In this study, our aim was to asses the redox status in occupationally silica-exposed workers, by evaluating the dynamic thiol-disulphide homeostasis. STUDY DESIGN: Case-control study. METHODS: Thirty-six male workers occupationally exposed to silica particles and 30 healthy volunteers, working as office workers were included to the study. Posteroanterior chest radiographs and pulmonary function tests of both groups were evaluated. Also serum thiol disulphide levels were measured using the spectrophotometric method described by Erel and Neselioglu. RESULTS: Among the 36 workers that underwent pulmonary function tests 6 (17%) had obstructive, 7 (19%) had restrictive, 6 (17%) had obstructive and restrictive signs whereas 17 (47%) had no signs. The mean PFTs results of silica-exposed workers were significantly lower than control subjects. The serum disulphide levels of silica-exposed workers were significantly higher than control subjects (23.84±5.89 µmol/L and 21.18±3.44 µmol/L, respectively p=0.02). CONCLUSION: The serum disulphide levels, a biomarker of oxidative stress, are found to be higher in silica-exposed workers.

Dynamic disulfide/thiol homeostasis in lead exposure denoted by a novel method.

Lead is a toxic heavy metal, and prevention of human exposure to lead has not been accomplished yet. The toxicity of lead is continually being investigated, and the molecular mechanisms of its toxicity are still being revealed. In this study, we used a novel method to examine thiol (SH)/disulfide homeostasis in workers who were occupationally exposed to lead. A total of 80 such workers and 70 control subjects were evaluated, and their native and total SH values were measured in serum using a novel method; their blood lead levels were also assessed. The novel method used for SH measurements was based on the principle of measuring native SH, after which disulfide bonds were reduced and total SHs were measured. These measurements allowed us to calculate disulfide amounts, disulfide/total SH percent ratios, disulfide/native SH percent ratios, and native SH /total SH percent ratios. We found that disulfide levels were significantly higher in workers who were exposed to lead (21.08(11.1-53.6) vs. 17.9(1.7-25), p < 0.001). Additionally, the disulfide/native SH and disulfide/total SH percent ratios were higher in exposed workers, while the native SH/total SH percent ratios were higher in the control subjects. Furthermore, the lead and disulfide levels showed a positive correlation, with p < 0.001 and a correlation coefficient of 0.378. Finally, the novel method used in this study successfully showed a switch from SH to disulfide after lead exposure, and the method is fully automated, easy, cheap, reliable, and reproducible. Use of this method in future cases may provide valuable insights into the management of lead exposure.

Thiol/disulfide homeostasis in asphalt workers.

The aim of this study was to investigate thiol/disulfide homeostasis in asphalt workers who are exposed to polycyclic aromatic hydrocarbons occupationally. The study was carried out in 34 nonsmoker asphalt workers. Additionally, 35 healthy nonsmoker volunteers were recruited as control group. Thiol and disulfide concentrations were determined using the novel automated measurement method. Levels of urinary 1-OH-pyrene were analyzed by liquid chromatography. Disulfide/thiol ratio was significantly higher in exposed group (p = .034). Also, a positive correlation was detected between disulfide/thiol ratio and 1-OH-pyrene values (r = .249, p = .036). Thiol/disulfide homeostasis was found to be disturbed in asphalt workers. The novel test used in this study may be useful for evaluating the oxidative status in polycyclic aromatic hydrocarbon (PAH) exposure.

Antinociceptive Effect of Mirtazapine in Rats with Diabetic Neuropathy.

INTRODUCTION: To evaluate the antinociceptive effect of mirtazapine and the mechanisms mediating this effect in neuropathic pain in rats with diabetes. METHODS: The experiments were performed in Sprague Dawley rats using a hot-plate device. Streptozotocin (STZ) was administered to the rats after taking control measurements. Rats with a blood glucose level of 240 mg/dL or above in the blood specimen obtained from the tail vein 3 days after STZ administration were considered as being diabetic. Three weeks after STZ administration, the hot-plate test was performed. Compared with the control measurements, rats that exhibited >20% decrease in the second hot-plate test measurements were considered to have developed neuropathy. Drugs [mirtazapine, naloxone (opioidergic antagonist), metergoline (serotonergic antagonist), and BRL44408 (adrenergic antagonist)] and drug combinations were administered to those rats that developed neuropathy. After administrating the drugs or drug combinations, the third hot-plate test was performed. RESULTS: Mirtazapine at doses of 10 and 15 mg/kg exhibited a significant antinociceptive effect. Naloxone, metergoline, or BRL44408 alone did not cause an antinociceptive effect. However, combinations of these drugs with mirtazapine (15 mg/kg) significantly decreased the antinociceptive effect of mirtazapine. CONCLUSION: It is suggested that mirtazapine has a significant antinociceptive effect in diabetic neuropathy and that opioidergic, serotonergic, and adrenergic systems have roles to play in this effect.

[Low doses of prazosin potantiates the antinociceptive/analgesic effect of amitriptyline]. / Düsük doz prazosin amitriptilin'in antinosiseptif/analjezik etkisini potansiyalize ediyor.

In this study, we aimed to reveal the interaction between the tricyclic antidepressant amitriptyline and a1-adrenoceptor antagonist prazosin in mice by using an analgesiometric device hot-plate. Amitriptyline (10 mg/kg) has analgesic effect as expected. Neither of the prazosin doses (0.1, 0.2, 0.5, 1 mg/kg) displayed analgesic effect alone. The combination of lower doses of prazosin (0.1, 0.2, 0.5 mg/kg) with amitriptyline (10 mg/kg) potentiated the antinociceptive effect of this drug. However, the relatively higher dose of prazosin (1 mg/kg) did not effect amitriptyline analgesia. Thus we conclude that the antinociceptive effect of amitriptyline is potentiated by low doses of prazosin.