Evaluation of the effect of cannabidiol on the THLE-2 liver cell line exposed to lead.

Environmental and soil pollution increase the likelihood of human exposure to toxic metals. Therefore, there is a need for new methods and substances to protect individuals against the harmful effects caused by toxic metals. The study is the first to aim at determining the protective effect of cannabidiol (CBD) against oxidative stress and inflammation induced by toxic metal exposure in Transformed Human Liver Epithelial-2 (THLE-2) cell lines representing healthy liver cells. The IC50 value was determined by exposing THLE-2 human liver healthy cell line to different molarities of lead (Pb) using the XTT kit. The protective efficacy of CBD was assessed by adding 5 µM CBD in addition to the Pb doses determined at IC50 levels to the Pb groups created in cell lines. The levels of GSH, MDA, MPO, CAT, TNF-α, IL-1ß, and IL-6 in cell lines were determined using ELISA kits. The inhibition of toxic metal entry into the cells by CBD was assessed through ICP-MS analysis. The IC50 value for Pb was determined as 10 µM in 2D cell lines and 25 µM in 3D cell lines. It was observed that the application of 5 µM concentration of CBD, along with the determined IC50 doses for Pb, increased the cell proliferation rate. Furthermore, the decrease in GSH and CAT levels and the increase in MDA, MPO, TNF-α, IL-1ß, and IL-6 levels observed in cell lines treated only with Pb were reversed with the application of CBD. The ICP-MS analysis revealed that CBD reduced the cellular uptake of Pb. The reversal of oxidative stress and inflammation induced by Pb, the increase in cell proliferation, and the reduction in the cellular uptake of toxic metals by CBD can be considered as strong evidence for the protective use of CBD in Pb exposures.

A mechanistic review of pharmacological activities of homeopathic medicine licorice against neural diseases.

The use of medicinal plants has grown in popularity in recent decades because, as natural ingredients, they have fewer adverse effects and are more effective than synthetic alternatives. As a small perennial herb, Glycyrrhiza glabra L. (Licorice) has been investigated for its therapeutic efficacy against neural disorders mainly ischemic stroke as well as the neurodegenerative diseases such as dementia and Alzheimer's disease, and Parkinson's disease which has been attributed to its HMGB inhibitory function, reactive oxygen scavenging and anti-inflammatory activity. The objective of current review is to review the evidence for the pharmacological effects of licorice and its vital active components on neurological disorders and the underlying signaling networks. We reviewed Papers published from 2000.1.1 up to 2 January 2023 in web of science, Google Scholar and PubMed data bases using key words including "Licorice," "Glycyrrhiza glabra L.," "Glycyrrhizic acid," "brain," "neurodegenerative disease," "Alzheimer's," and "Parkinson" were used to search in title/abstracts. Licorice extract and/or its active components can be used safely in therapeutic doses for optimizing the management of a multiple neurodegenerative disorders, and hampering the extent of neural tissue injury and neurologic deficits subsequent to cerebrovascular accidents.

Analyses of interleukin-6, presepsin and pentraxin-3 in the diagnosis and severity of late-onset preeclampsia.

INTRODUCTION: The etiology/pathophysiology of preeclampsia remains an enigma. Maternal inflammation (humoral and cellular) is a key factor in the etiology of late-onset preeclampsia (L-PrE). Presepsin is split out from the phagocytes membranes after phagocytosis. It is known as a novel inflammation marker. To our knowledge, this is the first study in literature in English to investigate maternal blood concentrations of presepsin in preeclampsia and healthy pregnant women. METHODS: We examined maternal plasma interleukin-6, presepsin and pentraxin-3 concentrations in pregnant women with (n = 44) and without L-PrE (n = 44). These three inflammatory markers concentrations measured using enzyme-linked immunosorbent assays were compared. RESULTS: The mean maternal age and gestational age at sampling are similar in the both groups (p ≥ .05). Interleukin-6, presepsin and pentraxin-3 concentrations differed between the groups (p < .05). There was no difference between the three inflammatory markers concentrations in patients with mild (22 patients) and severe (22 patients) preeclampsia in L-PrE (p ≥ .05). A significant discriminative role of interleukin-6, presepsin and pentraxin-3 for presence of L-PrE, with cutoff values of 39.74 pg/mL, 309.88 mg/L and 34.96 ng/mL, respectively, were reported in a ROC curve analysis. When the patients with and without small for gestational age infants (12 patients and 76 patients, respectively) were compared, it was determined that there was no differences between the interleukin-6, but there were differences between the presepsin and pentraxin-3 concentrations (p = .016, p = .008, respectively). CONCLUSION: Lower concentrations of interleukin-6/presepsin and higher concentrations of pentraxin-3 were associated with the development of preeclampsia. Further investigations of inflammatory/immunity markers in pregnancy are required and may ultimately lead to novel therapeutic approaches to treat complications of pregnancy.

Measuring the status of maternal serum thiol/disulfide couples in the diagnosis and/or the determination of the severity of late-onset preeclampsia.

OBJECTIVE: Preeclampsia (PrE) is a pregnancy-related disorder. PrE affects the health of the mother and/or the fetus binomial with short and/or long-term consequences. The role of oxidant/antioxidant molecules and aberrant maternal inflammation in PrE has been documented. However, the importance of antioxidant molecules such as thiols has been poorly documented. In this research, a possible link between serum thiols levels and the diagnosis/severity of late-onset PrE (L-PrE) was investigated. MATERIALS AND METHODS: We examined maternal serum native thiols, disulfide, total thiols levels, and their ratios in pregnant women with (n = 51) and without L-PrE (n = 50). The levels of these three markers were measured using spectrophotometric assays and compared. RESULTS: There were significant differences in terms of serum native and total thiols levels between patients with L-PrE and healthy pregnant women (p = .001, p = .008, respectively). Disulfide levels were not different in either group (p = 0.729). There was no difference between total thiols, native thiols, disulfide concentrations, and their ratios in patients with mild (23 patients) and severe (27 patients) preeclampsia in L-PrE (p ≥ .05). A significant discriminative role of native and total thiols for the presence of L-PrE, with cutoff values of 175.86 µmol/L and 296.73 µmol/L, respectively, were revealed in ROC curve analysis. CONCLUSIONS: Lower concentrations of total/native thiols were linked with the development of L-PrE. However, there is still a need for more clinically useful biomarkers/molecules and management strategies in PrE.

Analyses of maternal plasma cadmium, lead, and vanadium levels in the diagnosis and severity of late-onset preeclampsia: a prospective and comparative study.

INTRODUCTION: Cadmium, lead, and vanadium, important pollutants produced from anthropogenic activities, have been suggested to be embryotoxic and fetotoxic in many studies. However, the causes of preeclampsia are little known and heavy metals merit further investigation. We tested whether late-onset preeclampsia (L-PrE) was associated with exposure to these metals. METHODS: This study was designed to determine maternal plasma cadmium, lead, and vanadium concentrations in women with L-PrE (n = 46) compared with those of normotensive women (n = 46). The concentrations of the metals were measured using inductively coupled plasma-mass spectrometry and compared. RESULTS: The groups were matched for maternal age, gestational age, and gravidity (p ≥ 0.05). Vanadium concentrations differed between the groups (p = 0.007). In contrast, there were no significant differences in the concentrations of cadmium and lead between the groups (p ≥ 0.05). There was no difference between the concentrations of the metals in patients with mild (n = 23) and severe (n = 23) preeclampsia in L-PrE (p ≥ 0.05). A significant discriminative role of vanadium for the presence of L-PrE, with a cutoff value of 1.84 µg/L, was found in ROC curve analysis. When the patients with and without small-for-gestational-age infants were compared (n = 12, and n = 80, respectively), it was determined that there were no differences between cadmium, lead, and vanadium concentrations (p ≥ 0.05). CONCLUSION: Lower levels of vanadium might be associated with the development of L-PrE. Our findings require further investigation in other populations.

Selenium, Zinc, and Copper Status in Euthyroid Nodular Goiter: A Cross-Sectional Study.

BACKGROUND: It is known that some elements are needed for normal thyroid gland functions. Iodine and selenium are the most well-known trace elements necessary for thyroid metabolism. Selenium is involved in the formation of thyroid hormones and the structure of the deiodinases associated with the development of the thyroid gland. While the role of zinc in thyroid metabolism is at the T3 receptor level, the role of copper is yet not clear. OBJECTIVE: To compare the levels of serum trace elements such as selenium, zinc, and copper between the patients with euthyroid nodular goiter and healthy participants. METHODS: This cross-sectional study included 98 patients with euthyroid multinodular goiter and 83 healthy subjects without thyroid disease. The demographics, thyroid hormone levels, and thyroid ultrasonography of the participants were recorded. Venous blood samples were centrifuged and sera samples were stored at -80°C until analysis of selenium, zinc, and copper levels. The levels of trace elements were determined by inductively coupled plasma-mass spectrometry (ICP-MS). RESULTS: While serum, zinc, and selenium levels were significantly higher in the control group than the nodular goiter group, the copper levels were similar in the two groups. Trace elements were not correlated with thyroid hormone levels and thyroid volumes. Patients in the nodular goiter group were analyzed according to their solitary and multiple nodule status. The solitary and multiple nodular goiter groups were similar in terms of copper, zinc, and selenium levels. CONCLUSIONS: Deficiency of selenium and zinc may be associated with nodular goiter. Replacement of these trace elements may be useful for the prevention of nodular goiter, especially in deficient regions.

Assessment of potential cardiovascular risk in trichloroethylene exposure by serum methylated arginine levels.

Trichloroethylene (TCE) is a widely used solvent in industrial applications and has toxic effects on various systems. Methylated arginine amino acids (eg asymmetric dimethyl arginine (ADMA), symmetric dimethyl arginine (SDMA)) cause the development of cardiovascular disease by inhibiting NO synthesis, which is considered to be heart-protector. The aim of this study is to determine the risk of cardiovascular diseases in TCE exposure by methylated arginine biomarkers. About 98 controls and 100 TCE-exposed male subjects were included in the study. Trichloroacetic acid (urinary metabolite of TCE), arginine, homoarginine, citrulline ADMA, SDMA, and N-monomethyl L-arginine (L-NMMA) levels were found significantly higher than control group (p < 0.001). The strongest correlation was found between ADMA and Trichloroacetic acid (TCA) level (r = 0.453, p < 0.01). Long-term TCE exposure, may be an important risk factor for cardiovascular diseases by increasing methylated arginine levels.

The relationship between impaired lung functions and cytokine levels in formaldehyde exposure.

Exposure to formaldehyde (FA) causes detrimental effects on respiratory system. Inflammation is one of the mechanisms responsible for these effects. Our aim is to demonstrate the possible effect of formaldehyde on inflammation biomarkers and pulmonary function tests. One hundred ninety-eight male workers in a fiber production factory are included. Eighty two of them were not exposed to FA. Thirty nine workers were exposed to FA for 4 h or more in a work shift and 77 workers were exposed less than 4 h. Statistically significant differences were found for FA, TNF-α, and IL-6 levels and pulmonary function test parameters (FEV1 and FVC) between no exposure and exposure groups. The results revealed a correlation between decrement in pulmonary function tests and an increase in cytokine levels concordant with the duration of FA exposure. The results may emphasize that FA exposure shows its effect on pulmonary system via inflammatory pathways.

The Relationship Between Heavy Metal Exposure, Trace Element Level, and Monocyte to HDL Cholesterol Ratio with Gestational Diabetes Mellitus.

The objective of this study is to assess the levels of heavy metals (cadmium, lead, antimony, mercury, and arsenic), which are also called endocrine-disrupting chemicals, and trace elements (chromium-III, chromium-VI, zinc, copper, and selenium) vs. monocyte to HDL ratio among pregnant women with gestational diabetes mellitus (GDM). A total of 112 pregnant women (60 with GDM and 52 healthy women) were included in this case-control study. Analysis of heavy metals and trace elements were performed in inductively coupled plasma mass spectrometer. Heavy metals (cadmium, lead, antimony, mercury, and arsenic), trace elements (chromium-III, chromium-VI, zinc, copper, and selenium), and metabolic parameters were assessed in both groups. It was determined that the levels of cadmium, lead, antimony, and copper were higher (p < 0.05) and levels of chromium-III, zinc, and selenium were lower (p < 0.05) among the GDM group compared to the control group, whereas there was a statistically insignificant difference between the two groups, regarding the levels of copper, mercury, and arsenic (p > 0.05). Moreover, the monocyte to HDL ratio was higher in the GDM group (p < 0.05), and the insulin resistance was significantly higher as well (p < 0.05). The results of our study demonstrated that environmental factors could be effective in the etiology of GDM. Toxic heavy metals, through inducing Cu, OS, and chronic inflammation, and other trace elements, either directly by impacting insulin secretion or through weakening the body's antioxidant defense system, could play a role in the occurrence of GDM.

Environmental Exposures in the Etiology of Abortion: Placental Toxic and Trace Element Levels.

PURPOSE: Intensive research has been conducted on the effects of toxic and trace elements on pregnancy. Previous studies indicated a possible relationship between placental levels of these elements and first-trimester abortion; however, their effects on the further gestational weeks are not clear. This study aimed to investigate the effect of changes in the levels of placental trace and toxic elements on second-trimester abortion. METHODS: The patient group consisted of 30 women with missed abortion. The control group comprised 60 healthy term and singleton pregnant women who gave birth. Placental samples were obtained from the patients and the healthy controls, and the concentrations of placental elements were measured using inductively coupled plasma mass spectrometry. RESULTS: In the abortion group, placental arsenic, cadmium, mercury, lead, antimony, tin, cobalt, manganese, and selenium levels were significantly higher than those of the control group (p<0.05). Antimony was determined as an independent predictor with an odds ratio of 6.1 in toxic elements (p=0.025), and selenium was determined as an independent predictor with an odds ratio of 2.3 in trace elements (p=0.015). CONCLUSION: The changes in trace element and toxic element levels, especially an increase in antimony and selenium, in placental tissue due to environmental exposure may play an important role in second-trimester abortion.

Are Heavy Metal Exposure and Trace Element Levels Related to Metabolic and Endocrine Problems in Polycystic Ovary Syndrome?

This study aimed to determine the relationship between the metabolic and endocrinological pathologies in polycystic ovary syndrome (PCOS) and the levels of arsenic, chromium, cadmium, lead, mercury, antimony, zinc, and copper to evaluate the relationship of these toxic metals with inflammatory/oxidative parameters. This study included a total of 154 patients (84 with PCOS, 70 healthy volunteers). Metabolic and endocrine parameters and arsenic, chromium, cadmium, lead, mercury, antimony, zinc, and copper serum levels of the patients were compared between the groups. Considering the action mechanism of toxic metals, serum malondialdehyde (MDA), superoxide dismutase (SOD), serum total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), tumor necrosis factor-alpha (TNFα), and high-sensitivity C-reactive protein (HsCRP) levels were determined. Serum TAS (p = 0.002), OSI (p = 0.006), SOD (p = 0.006), zinc (p = 0.010), and copper (p = 0.030) values were statistically lower whereas TOS (p = 0.008), MDA (p < 0.001), HsCRP (p < 0.001), TNFα (p < 0.001), antimony (p < 0.001), cadmium (p < 0.001), lead (p < 0.001), and mercury (p < 0.001) levels were significantly higher in the PCOS group than those determined in the control group. Antimony was positively correlated with fasting glucose (FG) and HOMA-IR while cadmium, in addition to FG and HOMA-IR, positively correlated with insulin and lead had a positive correlation only with FG (p < 0.05). Also, these three heavy metals correlated positively with some oxidative system and inflammatory parameters and negatively with the antioxidant system parameters (p < 0.05). In conclusion, heavy metal exposures in PCOS may be related to insulin resistance and hirsutism through oxidative and inflammatory mechanisms. This approach can be used to identify the risky patient group and to develop new treatment modalities.

Effects of quercetin loaded nanostructured lipid carriers on the paraquat-induced toxicity in human lymphocytes.

Paraquat (PQ) as a herbicide and an environmental pollutant with increasing importance due to its toxicity to humans and animals. This study aimed to evaluate the protective and antioxidant activity of quercetin loaded Nanostructured Lipid Carriers (QNLC) against toxicity induced by PQ. Blood lymphocytes were prepared using Ficoll polysaccharide and subsequently by gradient centrifugation. The QNLC was prepared using an ultra-sonication method, which was characterized by dynamic light scattering (DLS) and transmission electron microscopy (TEM). The viability, reactive oxygen species (ROS), lipid peroxidation (LPO), mitochondrial membrane potential (MMP), lysosome membrane integrity, Bax and Bcl2 gene expression were evaluated in human isolated lymphocytes. The results showed spherical QNLCs with nano-size range (52.7 nm) and high drug encapsulation efficiency (98.5% -96%). The results also indicated that PQ induced cell death, as well as ROS production, decreased by QNLC in human lymphocytes. Also, QNLC meaningfully restored MMP reduction, lysosomal membrane destabilization, and lipid peroxidation and were capable of preventing PQ-treated change in Bax and Bcl2 gene expression. We report that QNLC, have a significantly higher capacity to prevent PQ-induced toxicity than Q itself. It is suggested that the QNLC is a promising antioxidant for drug delivery to be used as a therapeutic and prophylactic agent for PQ poisoning.

Simultaneous quantitative detection of 10 phthalates in PVC children's toys by HPLC-PDA.

A high-performance chromatography-photodiode array detection (HPLC-PAD) method has been developed and validated for the identification and quantification of ten phthalates; diethyl phthalate (DEP), diallyl phthalate (DAP), benzyl butyl phthalate (BBP), di-n-butyl phthalate (DBP), dihexyl phthalate (DHP), dicyclohexyl phthalate (DCHP), di-2-ethylhexyl phthalate (DEHP), di-n-octyl phthalate (DOP), diisononyl phthalate (DINP) and diisodecyl phthalate (DIDP) in children's PVC toys. The phthalates were extracted from PVC toy sample using ultrasonic extraction with methanol. Quantification analysis was achieved by gradient elution mode using reversed-phase ODS-4 C18 column with PAD detection at 226 nm. The method has been validated for (BBP, DOP, DINP, and DIDP) and (DEP, DAP, DBP, DCHP, DHP, and DEHP) in the concentration range of 1-100 and 2-200 mg L-1, respectively. The accuracy determined as recovery were 82.85-107.40% with RSD values at 0.8-4.2%. The limits of detection for (DEP, DAP, BBP, DBP, DCHP, DHP, DEHP, DOP, DINP, and DIDP) were 0.02, 0.04, 0.01, 0.03, 0.02, 0.03, 0.03, 0.01, 0.08, and 0.10 mg L-1, respectively.

Changing levels of selenium and zinc in cadmium-exposed workers: probable association with the intensity of inflammation.

Inflammation is a response mediated by multiple cytokines, such as IL-6, IL-10 and TNF-α. Cadmium (Cd) has been involved in the etiopathogenesis of many diseases via inflammation. Selenium (Se) and zinc (Zn) play a pivotal role in maintaining many physiological functions of cells as well as inhibiting Cd-induced cytotoxicity. This study investigated the anti-inflammatory effects of Se and Zn in cadmium-exposed workers by measuring the levels of IL-6, IL-10 and TNF-α cytokines in 68 control and 91 Cd-exposed subjects. Blood samples were obtained from each participant for immunological, toxicological and routine analysis. All samples were digested by microwave oven and analysed by inductively coupled plasma mass spectrometry (ICP-MS). IL-6, IL-10 and TNF-α cytokine levels were found to be statistically different (p < 0.001) between the control and Cd-exposed groups (23.50 ± 7.70 pg/mL vs. 69.05 ± 19.06 pg/mL; 28.61 ± 9.83 pg/mL vs. 51.79 ± 11.77 pg/mL; 3.44 ± 1.14 pg/mL vs. 5.79 ± 1.04 pg/mL, respectively). High positive correlations were found between Cd levels of participants and IL-6, IL-10, TNF-α and CRP levels (r = 0.568, r = 0.615, r = 0.614 and r = 0.296, respectively, p < 0.01). In terms of the regression analysis results, there were significant effects of Cd on IL-6, IL-10 and TNF-α levels (p < 0.05). The Cd, Zn and Se levels between control and exposed group were significantly different [0.26 ± 0.15 µg/L vs. 3.36 ± 1.80 µg/L; 143.91 ± 71.13 µg/dL vs. 121.09 ± 59.88 µg/dL; 92.98 ± 17.03 µg/L vs. 82.72 ± 34.46 µg/L (p < 0.001, p < 0.03, p < 0.015), respectively]. In conclusion, increasing levels of Se and Zn decreases the intensity of inflammation as measured by IL-6, IL-10 and TNF-α levels.

The effects of barnidipine on an experimental ischemia reperfusion model of spinal cord injury and comparison with methyl prednisolone.

OBJECTIVE: Increased intracellular calcium concentration plays an important role in the secondary mechanism of spinal cord injury. In the presenting experimental study, we aimed to evaluate the healing effect of barnidipine, which has a high affinity for L-type calcium channels, on acute spinal cord injury and to compare its effects with those of methylprednisolone. METHODS: A total of 32 Spraque Dawley albino adult female rats were divided into 4 groups; group 1: sham-operated (n=8), group 2: only ischemia (n=6), group 3: barnidipine-treated (n=8), and group 4: methylprednisolone-treated (n=6). An ischemia-reperfusion model was created by clipping the abdominal aorta in the rats. Motor examination was performed 1 hour after the surgical procedure and before sacrification. Immediately following the second motor examination, rats were sacrificed and tissue samples were taken for histopathological examination and for testing of tissue malondialdehyde (MDA) levels. RESULTS: A significant correlation of motor examination was found between the sham-operated and barnidipine-treated groups and the sham-operated and only ischemia groups at the 1st and 24th hour (p<0.008). There was no significant difference between the only ischemia and barnidipine-treated groups and only ischemia and methylprednisolone-treated groups (p>0.008). Light microscopic examination of the sham-operated group revealed findings consistent with normal spinal cord structure. In group 2, 3, and 4, light microscopic examination revealed polymorphonuclear leukocyte infiltration and a small amount of axonal swelling. There was no significant correlation between the ischemia and barnidipine-treated groups and the barnidipine and methylprednisolone groups in terms of MDA levels (p>0.008). CONCLUSION: A single dose of barnidipine (10 mg/kg) and methylprednisolone are not effective and not sufficient to prevent spinal ischemia-reperfusion injury in rats.

TNF-α and IL-6 as Biomarkers of Impaired Lung Functions in Dimethylacetamide Exposure.

BACKGROUND: Tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) are well-known biomarkers of systemic inflammation that have been associated with many diseases in the past. In this study, we aimed to determine the relationship between impaired lung functions and the levels of these biomarkers in DMAc exposed people. METHODS: 101 non-exposed control subjects (Group 1) and 109 DMAc-exposed workers from the polyvinyl chloride (PVC) industry were included in the study. In the next step, the exposed group was divided into two groups according to the level of exposure (Group 2 and 3). DMAc, TNF-α, IL-6, creatinine, ALT, AST, GFR and standard spirometry measurements were carried out in all subjects. RESULTS: When compared to the control group, TNF-α and IL-6 levels were significantly high compatible with the increase of DMAc levels, in the exposed groups. Urinary DMAc Levels were 0.06 mg/L in the control group. This level is significantly low when compared to exposed and severely exposed group (2.43 mg/L and 3.17 mg/L). TNF-α levels were 56.86 pg/mL, 145.52 pg/mL and 230.52 pg/mL in control, exposed and severely exposed groups. IL-6 levels were found to be 38.08 pg/mL, 89.19 pg/mL and 116 pg/mL for control, exposed and severely exposed groups, respectively. Similarly, the FEV1/FVC ratio decreased especially in the severely exposed group (p 0.001). CONCLUSIONS: In our study, results have revealed that TNF-and IL-6 levels are promising biomarkers in the early diagnosis of lung function impairment in inhalational DMAc exposure.

The effects of occupational lead exposure on selected inflammatory biomarkers.

In exposure to toxic metals such as lead, determining lead and cytokine levels (IL-6, IL-10, and TNF-α) is essential for early detection of diseases. The aim of this study was to develop an model for early detection of inflammation and onset of atherosclerosis in the absence of clinical findings in young workers, which could help physicians take timely an action and start treatment. This study included 49 metal workers exposed to lead occupationally and 50 unexposed administrative workers (controls) who underwent immunological analysis for cytokines (IL-6, IL-10, and TNF-α) and atherosclerosis markers (h-FABP and VCAM-1), toxicological analysis for lead, and routine biochemical analysis (ALT, AST, creatinine) at the Ankara Occupational and Environmental Diseases Hospital in 2017. Lead levels correlated with IL-6, IL-10, and TNF-α (r=0.469, r=0.521 and r=0.279, respectively, p<0.01) but did not significantly affect h-FABP and VCAM-1 levels.

Arsenic-induced inflammation in workers.

Occupational and environmental exposures to metal and metalloids can result in neurotoxicity and immunotoxicity. Selenium (Se) is essential for the proper functioning of neutrophils, macrophages, natural killer (NK) cells, T-lymphocytes and other immune mechanisms, while zinc (Zn) is a trace element essential for basic cell activities, including cell growth and differentiation. Arsenic (As) may lead to different types of immunosuppressive effects. This study consisted of 62 male workers, who had been exposed to arsenic for different durations and 73 non-exposed male workers (control group) with no history of occupational toxic metal exposure. Whole blood and serum samples were taken from each participant for immunological, toxicological and routine analysis during their annual periodical examination. Arsenic, selenium and zinc levels were determined by the ICP-MS and cytokines, IL-6, IL-10, TNF-α, sE-selectin and VCAM-1, were measured by ELISA. There were statistically significant differences (p < 0.001) between control and As-exposed group in As (1.37 ± 0.42 vs. 4.27 ± 1.54 µg/L) and Se levels (106.37 ± 48.04 vs. 74.70 ± 30.45 µg/L). The changing levels of As, Zn and Se seems to affect the severity of inflammatory reactions based on IL-6, IL-10 and TNF-α levels (r = 0.755, r = 0.679 and r = 0.617, respectively, for all p < 0.01). Selenium was found to have a suppressive effect on cytokines, as evidenced by Pearson correlations and regression analysis. These findings support the need to closely monitor Se levels in individuals exposed to arsenic and benefits for Se supplementation in the case of arsenic exposure, occupationally or environmentally.