A newly developed consortium with a highly efficient thiocyanate degradation capacity: A comprehensive investigation of the degradation and detoxification potential.

Thiocyanate-containing wastewater harms ecosystems and can cause serious damage to animals and plants, so it is urgent to treat it effectively. In this study, a new efficient thiocyanate-degrading consortium was developed and its degradation characteristics were studied. It was found that up to 154.64 mM thiocyanate could be completely degraded by this consortium over 6 days of incubation, with a maximum degradation rate of 1.53 mM h-1. High-throughput sequencing analysis showed that Thiobacillus (77.78%) was the predominant thiocyanate-degrading bacterial genus. Plant toxicology tests showed that the germination index of mung bean and rice seeds cultured with media obtained after thiocyanate degradation by the consortium increased by 94% and 84.83%, respectively, compared with the control group without thiocyanate degradation. Cytotoxicity tests showed that thiocyanate without degradation significantly decreased the Neuro-2a cell activity and mitochondrial membrane potential; induced reactive oxygen species generation and apoptosis; increased the cellular Ca2+ concentration; and damaged the cell nucleus and DNA. Furthermore, the thiocyanate degradation products produced the consortium were almost totally non-toxic, revealing the same characteristics as those of the control using distilled water. This study shows that the consortium has a high degradation efficiency and detoxification characteristics, as well as great application potential in bioremediation of industrial thiocyanate-containing wastewater.

Transcriptome reveals the crucial role of exogenous hydrogen sulfide in alleviation of thiocyanate (SCN-) toxicity in rice seedlings.

Application of exogenous hydrogen sulfide (H2S) is a novel strategy for alleviation of the adverse effects caused by abiotic stresses. However, little is known about H2S-mediated global molecular response of rice seedlings to thiocyanate (SCN-) exposure. Herein, a hydroponic experiment was carried out to investigate the crucial role of exogenous H2S in alleviation of SCN- toxicity generated at different effective concentrations (EC20: 24.0 mg SCN/L, EC50: 96.0 mg SCN/L, and EC75: 300.0 mg SCN/L) in rice seedlings through transcriptome analysis. The results showed that the total numbers of differentially expressed genes (DEGs, upregulated genes/downregulated genes) in rice roots were 755/313, 1114/3303, and 2184/7427, while they were 427/292, 2134/526, and 2378/890 in rice shoots at EC20, EC50, and EC75 of SCN-, respectively. When exogenous H2S was supplied to rice seedlings exposed to SCN-, the total number of DEGs (upregulated genes/downregulated genes) in rice roots was 1158/316, 1943/2959, and 1737/5392, while it was 2067/937, 2689/683, and 3492/1062 in rice shoots at EC20, EC50, and EC75 of SCN-, respectively. Upregulated DEGs in shoots were positively correlated with SCN- concentration in the presence of exogenous H2S, suggesting its crucial role in regulating the phytotoxicity of SCN-. Gene function and pathway enrichment analyses showed that exogenous H2S triggered "secondary metabolite synthesis," "metabolic pathways," and "signal transduction mechanisms" in rice seedlings corresponding to different effective concentrations of SCN- exposure.

Fuzzy synthetic evaluation of the impact of plant growth regulators on the root phenotype traits of rice seedlings under thiocyanate stress.

Application of plant growth regulators (PGRs) is a novel strategy for allay of the adverse effects caused by biotic/abiotic stresses. However, no studies have vividly executed mathematic evaluation for the assessment of various PGRs on root phenotype traits (RPTs) against pollutants. In the present study, a microcosm hydroponic experiment was conducted to examine responses of RPTs under SCN- (0, 24, 96, and 300 mg SCN/L) stress in the presence of PGRs such as jasmonic acid (JA), indole-3-acetic acid (IAA), and sodium hydrosulfide (NaHS) in rice plants. Fuzzy synthetic evaluation was applied to determine the outcome of the effects of various PGRs on the RPTs under SCN- exposure. Root scanning results indicated that exogenous IAA and NaHS has the greater potential for improving the RPTs of rice seedlings under SCN- stress, while JA failed to uplift the RPTs in response to SCN- stress. Fuzzy synthetic evaluation indicated that in control plants (without SCN-), the effect of three PGRs applied on the RPTs is as follows: NaHS > IAA > JA. At 24 mg SCN/L, NaHS and IAA had consistent actuate in regulating RPTs of rice seedlings, while all PGRs amended have an affirmative impact on RPTs at 96 and 300 mg SCN/L. The present research highlights the utilization of contemporary mathematic method to screen the superior species of PGRs through the RPTs test of plants under pollutant belt.

Familial Aggregation of Endemic Congenital Hypothyroidism Syndrome in Congo (DR): Historical Data.

Familial aggregation of endemic congenital hypothyroidism (CH) in an iodine-deficient population from northern Congo (Democratic Republic (DR)) was analysed on data collected four decades ago (1979-1980). During a systematic survey of 62 families, 46 endemic CH subjects (44 myxedematous and 2 neurological) were identified based on clinical evidence within a village cohort of 468 subjects. A distribution analysis showed that two families presented significant excess of cases versus a random background distribution. Both families were characterised by two healthy parents having all of their five offspring affected by some form of endemic CH. Goitre prevalence in endemic CH was lower than that in the general population, while goitre prevalence in the unaffected part of the cohort (parents and siblings) was similar to that of the general population. Some unidentified genetic/epigenetic factor(s) could contribute to the evolution of some iodine-deficient hypothyroid neonates through irreversible and progressive loss of thyroid functional capacity during early childhood (<5 years old). Besides severe iodine deficiency, environmental exposure to thiocyanate overload and selenium deficiency, factors not randomly distributed within families and population, intervened in the full expression of endemic CH. Further exploration in the field will remain open, as iodine deficiency in Congo (DR) was eliminated in the 1990s.

Environmental exposure to perchlorate, nitrate, and thiocyanate in relation to obesity: A population-based study.

BACKGROUND: Perchlorate, nitrate, and thiocyanate are well-known thyroid disrupters and may contribute to changes in body weight. However, the associations between environmental exposure to these chemicals and obesity-related outcomes remain unclear. OBJECTIVES: We aim to examine the urinary levels of perchlorate, nitrate, and thiocyanate and their associations with obesity and abdominal obesity in the U.S. METHODS: Here, we investigated the data of 16,265 adults aged 20-85 years from the National Health and Nutritional Examination Survey (NHANES) in 2001-2014. Urinary levels of perchlorate, nitrate, and thiocyanate were measured by ion chromatography combined with electrospray tandem mass spectrometry. Obesity and abdominal obesity were defined by the body mass index and waist circumference, respectively. Logistic regression models were used to estimate the associations. RESULTS: Overall, 5794 (35.6%) cases of obesity and 9090 cases (55.9%) of abdominal obesity were observed among the participants. In multivariable-adjusted logistic regression models, urinary nitrate was inversely associated with obesity (p = 0.0022 for trend), while urinary thiocyanate was positively related to obesity (p < 0.001 for trend). Compared with the lowest quartile, the odds ratios with 95% confidence intervals (CIs) across increasing quartiles were 0.95 (95% CI, 0.83-1.08), 0.88 (0.75-1.03), and 0.74 (0.60-0.90) for urinary nitrate and 1.31 (1.16-1.48), 1.53 (1.36-1.73), and 1.73 (1.47-2.03) for urinary thiocyanate. Urinary perchlorate was not correlated with obesity. Similar associations were also found between exposure to these chemicals and abdominal obesity. CONCLUSIONS: A higher exposure to urinary nitrate was associated with a lower risk of obesity, while a positive association was observed for urinary thiocyanate. These findings emphasize the need to longitudinally evaluate environmental exposure to perchlorate, nitrate, and thiocyanate with respect to their effect on obesity in humans.

Assessing effects of germline exposure to environmental toxicants by high-throughput screening in C. elegans.

Chemicals that are highly prevalent in our environment, such as phthalates and pesticides, have been linked to problems associated with reproductive health. However, rapid assessment of their impact on reproductive health and understanding how they cause such deleterious effects, remain challenging due to their fast-growing numbers and the limitations of various current toxicity assessment model systems. Here, we performed a high-throughput screen in C. elegans to identify chemicals inducing aneuploidy as a result of impaired germline function. We screened 46 chemicals that are widely present in our environment, but for which effects in the germline remain poorly understood. These included pesticides, phthalates, and chemicals used in hydraulic fracturing and crude oil processing. Of the 46 chemicals tested, 41% exhibited levels of aneuploidy higher than those detected for bisphenol A (BPA), an endocrine disruptor shown to affect meiosis, at concentrations correlating well with mammalian reproductive endpoints. We further examined three candidates eliciting aneuploidy: dibutyl phthalate (DBP), a likely endocrine disruptor and frequently used plasticizer, and the pesticides 2-(thiocyanomethylthio) benzothiazole (TCMTB) and permethrin. Exposure to these chemicals resulted in increased embryonic lethality, elevated DNA double-strand break (DSB) formation, activation of p53/CEP-1-dependent germ cell apoptosis, chromosomal abnormalities in oocytes at diakinesis, impaired chromosome segregation during early embryogenesis, and germline-specific alterations in gene expression. This study indicates that this high-throughput screening system is highly reliable for the identification of environmental chemicals inducing aneuploidy, and provides new insights into the impact of exposure to three widely used chemicals on meiosis and germline function.

Transcriptome analysis of Oryza sativa in responses to different concentrations of thiocyanate.

Effective concentrations of potassium thiocyanate (KSCN) to rice seedlings were experimentally determined using relative growth rate as a sensitive endpoint. Agilent 44-K rice microarray was used to profile the molecular responses of rice seedlings exposed to thiocyanate ion (SCN-) at three different effective concentrations (EC10, EC20, and EC50). A total of 18,498 known genes were collected from SCN-treated rice microarray analysis. Out of all, 1603, 1882, and 5085 differentially expressed genes (DEGs) were observed at EC10, EC20, and EC50 concentrations, respectively. More upregulated/downregulated DEGs were detected in shoots than in roots after SCN- exposure. Gene functions and pathway enrichment analysis of DEGs indicated that different effective concentrations of SCN- resulted in multiple enriched GO categories and KEGG pathways and outcomes were quite tissue-specific. Different regulations and adaptations of gene expression in molecular function (MF), biological process (BP), and cellular components (CC) were observed in rice tissues at different effective concentrations of SCN-, suggesting their different responsive and adaptive strategies. Information collected here presents a detailed description of SCN-induced alternations of gene expression in rice seedlings and provide valuable information for further searching specific genes participating in transportation, phytotoxic responses, and detoxification of SCN- in rice seedlings.

Characterization of the modes of action and dose-response relationship for thiocyanate on the thyroid hormone levels in rats using a computational approach.

Current practices for evaluating the cumulative risk of thyroid-active chemical mixtures (perchlorate, thiocyanate, nitrate) focus on the inhibition of thyroidal iodide uptake via the sodium iodide symporter (NIS) as the mode of action for potency equivalence calculations. However, unlike perchlorate, thiocyanate presents additional modes of action within the thyroid that could contribute to the overall thyroid perturbation. We tested the hypothesis of whether assuming a single mode of action of thyroidal iodide uptake inhibition is sufficient for describing the observed dose-response relationship for thiocyanate and its effects on serum thyroxine levels. An interaction model was developed by linking a biologically based dose-response model for iodide and thyroid hormones to a thiocyanate physiologically based pharmacokinetic model. Each model, adapted from the literature, was restructured and recalibrated in a Bayesian framework for the current mode of actions study. For a chronic exposure scenario, NIS inhibition alone was found not to be sufficient to describe the dose-response relationship for thiocyanate. Inclusion of additional modes of action involving iodide flux across the thyroid membrane and inhibition of iodide organification via thyroid peroxidase showed only moderate improvements in capturing the dose-response at environmental thiocyanate doses of exposure and failed to capture trends at very high doses. Our findings emphasize the need for more mechanistic data for chronic exposure scenarios to characterize better the overall dose-response relationship for thiocyanate. Risk assessment approaches for thyroid-active chemical mixtures that rely on NIS inhibition as the single mode of action may over-predict the contribution of thiocyanate to thyroid disruption.

In vitro comparative cytotoxicity study of a novel biocidal iodo-thiocyanate complex.

Novel biocides, which avoid the induction of cross-resistance to antibiotics, are an urgent societal requirement. Here, we compared the cytotoxic and bactericidal effects of a new antimicrobial agent, the iodo-thiocyanate complex (ITC), with those of the common antiseptics, hydrogen peroxide (H2O2), povidone iodine (PVP-I) and Lugol's iodine (Lugol). The antimicrobials were co-incubated for 10 min with HeLa and Escherichia coli cells in the presence and absence of organic matter (Dulbecco's modified Eagle's medium, supplemented with 10% fetal bovine serum). The cytotoxic concentrations of ITC were equivalent to its bactericidal concentrations (7.8 µg ml-1). By contrast, cytotoxic effects of H2O2, PVP-I and Lugol were apparent at concentrations lower than their bactericidal concentrations (250, 250 and 125 µg ml-1, respectively). The cellular effects of ITC were not quenched by organic matter, unlike the other antiseptics. ITC, PVP-I and Lugol had hemolytic effect on horse erythrocytes at high concentrations, while H2O2 showed no hemolysis. ITC, at 30 or 300 µg ml-1, did not cause DNA breakage in HeLa cells as assessed by an in vitro comet assay in the absence of S9 metabolic activation, whereas H2O2 caused extensive single-strand DNA breaks. The pronounced antimicrobial potency of ITC and its favorable cytotoxicity profile suggests that ITC should be considered for antiseptic applications.

Thiocyanate: a review and evaluation of the kinetics and the modes of action for thyroid hormone perturbations.

Exposure of the population to thiocyanate is predominantly through the diet and cigarette smoke. Thiocyanate is a potential thyroid disruptor due to its capacity to inhibit the uptake of iodide by the thyroid. Thiocyanate also interacts with the enzymatic reactions associated with iodide organification and thyroid hormone synthesis. Quantification of the dose-response relationships of thiocyanate and alteration in thyroid hormone levels is important for evaluating the risk of exposure to thiocyanate in humans. In this review, we highlight the key whole-body and intra-thyroidal aspects of thiocyanate kinetics in rats and its various modes of action for perturbing thyroid function. The inter-play between the various transporter- and enzyme-mediated modes of action contributes to the complexity in the dose-response relationship determinations for thiocyanate. We map the available modes of action in a mechanistic and quantitative manner. Findings summarized in this study can help support the development of a quantitative model to study the interaction effects of thiocyanate on the thyroid function. Additionally, the data gaps identified can help guide future experimental designs to characterize further thiocyanate dose-response. Finally, the strengths and weaknesses in current risk assessment considerations used for thiocyanate as a component of thyroid-active chemical mixtures are discussed.

Individual and combined inhibition of phenol and thiocyanate on microbial activity of partial nitritation.

This study evaluated the individual and interactive effect of phenol and thiocyanate (SCN-) on partial nitritation (PN) activity using batch test and response surface methodology. The IC50 of phenol and SCN- on PN sludge were 5.6 and 351 mg L-1, respectively. The PN sludge was insensitive to phenol and SCN- at levels lower than 1.77 and 43.3 mg L-1, respectively. A regression model equation was developed and validated to predict the relative specific respiration rate (RSRR) of PN sludge exposed to different phenol and SCN- concentrations. In the range of independent variables, the most severe inhibition was observed with a valley value (17%) for RSRR, when the phenol and SCN- concentrations were 4.08 and 198 mg L-1, respectively. An isobole plot was used to judge the combined toxicity of phenol and SCN-, and the joint inhibitory effect was variable depending on the composition and concentration of the toxic components. Furthermore, the toxic compounds showed independent effects, which is the most common type of combined toxicity.

The effect of smoking on placental pendrin expression.

Pendrin is important for transport of iodine across the placenta. Thiocyanate coming from cigarette is a competitive inhibitor of iodine transport. We aimed to evaluate the pendrin immunostaining intensity in placentas of smoker and non-smoker women. Placental tissues from 61 women, of which 28 were in smoking, and 33 were in non-smoking group were evaluated by immunohistochemical staining. Positive immunostaining was evaluated using a semiquantitative score: 0, negative; +, mild; ++, moderate; and +++, intense. Birth weight was significantly lower in the smoker group (p = 0.024). There was a negative correlation between birth weight and intensity of placental pendrin immunostaining in the smoker group (r = -0.44, p = 0.02). Placentas of the smoking women showed significantly higher immunostaining with pendrin than the control group (p = 0.006). Thiocyonate coming from cigarettes may competitively inhibit pendrin mediated iodine transport in the placenta and adversely affect foetal development by this mechanism.

Thyroid Antagonists (Perchlorate, Thiocyanate, and Nitrate) and Childhood Growth in a Longitudinal Study of U.S. Girls.

BACKGROUND: Perchlorate, thiocyanate, and nitrate are sodium/iodide symporter (NIS) inhibitors that block iodide uptake into the thyroid, thus affecting thyroid function. Thyroid dysfunction can adversely affect somatic growth and development in children. To our knowledge, no studies have examined effects of NIS inhibitors on body size measures. OBJECTIVE: We investigated associations between NIS inhibitors and childhood growth in 940 girls from the Puberty Study of the Breast Cancer and Environment Research Program. METHODS: Urine samples collected from girls 6-8 years of age at enrollment (2004-2007) from New York City, greater Cincinnati, Ohio, and the Bay Area in California were analyzed for NIS inhibitors and creatinine (C). The longitudinal association between NIS inhibitors and anthropometric measures [height, waist circumference, and body mass index (BMI)] during at least three visits was examined using mixed effects linear models, adjusted for race and site. RESULTS: Compared with girls in the low-exposure group (3.6, 626, and 500 mg/gC, median perchlorate, thiocyanate, and nitrate, respectively) girls with the highest NIS inhibitor exposure (9.6, 2,343, and 955 mg/gC, median perchlorate, thiocyanate, and nitrate, respectively) had slower growth in waist circumference and BMI but not height. Significant differences in the predicted mean waist circumference and BMI between the low- and high-exposure groups were observed beginning at 11 years of age. CONCLUSIONS: Higher NIS inhibitor exposure biomarkers were associated with reductions in waist circumference and BMI. These findings underscore the need to assess exposure to NIS inhibitors with respect to their influence on childhood growth. CITATION: Mervish NA, Pajak A, Teitelbaum SL, Pinney SM, Windham GC, Kushi LH, Biro FM, Valentin-Blasini L, Blount BC, Wolff MS, for the Breast Cancer and Environment Research Project (BCERP). 2016. Thyroid antagonists (perchlorate, thiocyanate, and nitrate) and childhood growth in a longitudinal study of U.S. girls. Environ Health Perspect 124:542-549; http://dx.doi.org/10.1289/ehp.1409309.

CO-occurring exposure to perchlorate, nitrate and thiocyanate alters thyroid function in healthy pregnant women.

BACKGROUND: Adequate maternal thyroid function during pregnancy is necessary for normal fetal brain development, making pregnancy a critical window of vulnerability to thyroid disrupting insults. Sodium/iodide symporter (NIS) inhibitors, namely perchlorate, nitrate, and thiocyanate, have been shown individually to competitively inhibit uptake of iodine by the thyroid. Several epidemiologic studies examined the association between these individual exposures and thyroid function. Few studies have examined the effect of this chemical mixture on thyroid function during pregnancy OBJECTIVES: We examined the cross sectional association between urinary perchlorate, thiocyanate and nitrate concentrations and thyroid function among healthy pregnant women living in New York City using weighted quantile sum (WQS) regression. METHODS: We measured thyroid stimulating hormone (TSH) and free thyroxine (FreeT4) in blood samples; perchlorate, thiocyanate, nitrate and iodide in urine samples collected from 284 pregnant women at 12 (±2.8) weeks gestation. We examined associations between urinary analyte concentrations and TSH or FreeT4 using linear regression or WQS adjusting for gestational age, urinary iodide and creatinine. RESULTS: Individual analyte concentrations in urine were significantly correlated (Spearman's r 0.4-0.5, p<0.001). Linear regression analyses did not suggest associations between individual concentrations and thyroid function. The WQS revealed a significant positive association between the weighted sum of urinary concentrations of the three analytes and increased TSH. Perchlorate had the largest weight in the index, indicating the largest contribution to the WQS. CONCLUSIONS: Co-exposure to perchlorate, nitrate and thiocyanate may alter maternal thyroid function, specifically TSH, during pregnancy.

Urinary thiocyanate concentrations are associated with adult cancer and lung problems: US NHANES, 2009-2012.

Links between environmental chemicals and human health have emerged but the effects from perchlorate, nitrate and thiocyanate were unclear. Therefore, it was aimed to study the relationships of urinary perchlorate, nitrate and thiocyanate concentrations and adult health conditions in a national and population-based study. Data was retrieved from US National Health and Nutrition Examination Surveys, 2009-2012, including demographics, blood pressure readings, self-reported health conditions and urinary perchlorate, nitrate and thiocyanate concentrations. Analyses included chi-square test, t test survey-weighted logistic regression models and population attributable risk estimation. There were no clear associations between urinary perchlorate concentrations and adult health conditions, although people with hearing loss and diabetes could be at the borderline risk. Urinary thiocyanate concentrations were significantly associated with emphysema (odds ratio (OR) 2.70 95% confidence intervals (CI) 1.91-3.82, P < 0.001), cancer (OR 1.21 95%CI 1.06-1.39, P = 0.008), chronic bronchitis (OR 1.23 95%CI 1.10-1.52, P = 0.003), wheezing (OR 1.24 95%CI 1.05-1.46, P = 0.011), coughing (OR 1.19 95%CI 1.03-1.37, P = 0.018) and sleep complaints (OR 1.14 95%CI 1.02-1.26, P = 0.019). The population attributable risks accounted for 3.3% (1.8-5.3%), 1.9% (0.6-3.5%), 1.2% (0.5-2.6%), 2.2% (0.5-4.1%), 1.8% (0.3-6.2%) and 1.3% (0.2-2.4%) for emphysema, cancer, chronic bronchitis, wheezing, coughing and sleep complaints, respectively. In addition, there was an inverse association observed between urinary nitrate level and heart failure. This is for the first time observing significant risk effects of urinary thiocyanate concentrations on adult cancer and lung problems, although the causality cannot be established. Elimination of such environmental chemical in humans should be included in future health policy and intervention programs.

Iodine deficiency, pollutant chemicals, and the thyroid: new information on an old problem.

Many women of reproductive age in the United States are marginally iodine deficient, perhaps because the salt in processed foods is not iodized. Iodine deficiency, per se, can interfere with normal brain development in their offspring; in addition, it increases vulnerability to the effects of certain environmental pollutants, such as nitrate, thiocyanate, and perchlorate. Although pregnant and lactating women should take a supplement containing adequate iodide, only about 15% do so. Such supplements, however, may not contain enough iodide and may not be labeled accurately. The American Thyroid Association recommends that pregnant and lactating women take a supplement with adequate iodide. The American Academy of Pediatrics recommends that pregnant and lactating women also avoid exposure to excess nitrate, which would usually occur from contaminated well water, and thiocyanate, which is in cigarette smoke. Perchlorate is currently a candidate for regulation as a water pollutant. The Environmental Protection Agency should proceed with appropriate regulation, and the Food and Drug Administration should address the mislabeling of the iodine content of prenatal/lactation supplements.

The association between perchlorate and thiocyanate exposure and thyroid function in first-trimester pregnant Thai women.

CONTEXT: Thyroid hormone is critical for fetal neurodevelopment. Perchlorate and thiocyanate decrease thyroidal iodine uptake by competitively inhibiting the sodium/iodide symporter. It is clear that perchlorate and thiocyanate anions can influence thyroid function. However, as pollutants in the environment, their impact is conflicting. OBJECTIVE: The objective was to determine the effects of environmental perchlorate and/or thiocyanate exposure on thyroid function in first-trimester pregnant women. DESIGN AND PATIENTS: A cross-sectional study was conducted in 200 pregnant Thai women with a gestational age of 14 weeks or less. MEASURES: Urinary iodide, perchlorate, thiocyanate, and serum thyroid function tests were measured. RESULTS: The women were aged 28.6 ± 6.1 years and the mean gestational age was 9.6 ± 2.7 weeks. Median urinary iodide, perchlorate, and thiocyanate concentrations were 153.5 µg/L, 1.9 µg/L, and 510.5 µg/L, respectively. Using Spearman's rank correlation analyses, there were positive correlations between serum TSH and urine perchlorate to creatinine (r = 0.20, P = .005) and TSH and thiocyanate to creatinine ratios (r = 0.22, P = .001). There were negative correlations between free T4 and the perchlorate to creatinine ratio (r = -0.18, P = .01) and free T4 and the thiocyanate to creatinine ratio (r = -0.19, P = .008). In multivariate analyses adjusting for log thiocyanate to creatinine ratio, log iodide to creatinine ratio, and gestational age, log perchlorate to creatinine ratio was positively associated with log TSH (P = .002) and inversely associated with log free T4 (P = .002). Log thiocyanate to creatinine ratio was a significant positive predictor of log TSH (P = .02) in women with a urine iodide level of less than 100 µg/L. CONCLUSIONS: Low-level environmental exposure to perchlorate and thiocyanate is common in Thailand. Low-level exposure to perchlorate is positively associated with TSH and negatively associated with free T4 in first-trimester pregnant women using multivariate analyses. In multivariate analyses, thiocyanate exposure is also positively associated with TSH in a subgroup of pregnant women with low iodine excretion.

Effect of maternal nicotine/thiocyanate exposure during gestational period upon pituitary, thyroid and parathyroid function/morphology of 1-month-old rat offspring.

INTRODUCTION: Impact of in utero exposure to nicotine, on the structure of the thyroid-pituitary axis and the parathyroid glands have been examined in 1-month-old rats and compared with that of thiocyanate. MATERIALS AND METHODS: Three pregnant female groups were used; control, nicotine and thiocyanate. Treatment started from gestation day (4-20) and the specimens were harvested from the male offspring of all groups at the age of 1 month and processed for light, electronmicroscopic and immunohistochemical examination. Total triiodothyronine (tT3), total thyroxine (tT4) and total thyrotropin (TSH) were quantitatively determined in serum. RESULTS: Both nicotine and thiocyanate activated the thyroid follicular cells, with an increase in height (about 30 %) and a negative feedback on the pituitary thyrotrophs which revealed a reduction in the number of cytoplasmic secretory granules, particularly the thiocyanate group. However, in thiocyanate group there was signs of impaired secretory activity of the thyroid gland. The arbitrary area of parathyroid chief cells, increased (about 45 %) particularly in nicotine group, with signs of reduced activity and a positive feedback on the parafollicular cells which revealed hypertrophy, proliferation (25 %) and increased intensity of positive immunohistochemical reaction for calcitonin. CONCLUSION: Nicotine impaired chief parathyroid cells activity and consequently activated parafollicular cells. Thiocyanate reduced pituitary thyrotrophs activity, whereas both nicotine and thiocyanate increased thyroid follicular cells activity. This impact of in utero exposure persisted for 1-month postnatal.

Microalgae-mediated simultaneous treatment of toxic thiocyanate and production of biodiesel.

In this work, a method for simultaneously degrading the toxic pollutant, thiocyanate, and producing microalgal lipids using mixed microbial communities was developed. Aerobic activated sludge was used as the seed culture and thiocyanate was used as the sole nitrogen source. Two cultivation methods were sequentially employed: a lithoautotrophic mode and a photoautotrophic mode. Thiocyanate hydrolysis and a nitrification was found to occur under the first (lithoautotrophic) condition, while the oxidized forms of nitrogen were assimilated by the photoautotrophic consortium and lipids were produced under the second condition. The final culture exhibited good settling efficiency (∼ 70% settling over 10 min), which can benefit downstream processing. The highest CO2 fixation rate and lipid productivity were observed with 2.5% and 5% CO2, respectively. The proposed integrated algal-bacterial system appears to be a feasible and even beneficial option for thiocyanate treatment and production of microbial lipids.

The smoking-associated oxidant hypothiocyanous acid induces endothelial nitric oxide synthase dysfunction.

Smokers have an elevated risk of cardiovascular disease but the origin(s) of this increased risk are incompletely defined. Considerable evidence supports an accumulation of the oxidant-generating enzyme MPO (myeloperoxidase) in the inflamed artery wall, and smokers have high levels of SCN(-), a preferred MPO substrate, with this resulting in HOSCN (hypothiocyanous acid) formation. We hypothesized that this thiol-specific oxidant may target the Zn(2+)-thiol cluster of eNOS (endothelial nitric oxide synthase), resulting in enzyme dysfunction and reduced formation of the critical signalling molecule NO•. Decreased NO• bioavailability is an early and critical event in atherogenesis, and HOSCN-mediated damage to eNOS may contribute to smoking-associated disease. In the present study it is shown that exposure of isolated eNOS to HOSCN or MPO/H2O2/SCN(-) decreased active dimeric eNOS levels, and increased inactive monomer and Zn(2+) release, compared with controls, HOCl (hypochlorous acid)- or MPO/H2O2/Cl(-)-treated samples. eNOS activity was increasingly compromised by MPO/H2O2/Cl(-) with increasing SCN(-) concentrations. Exposure of HCAEC (human coronary artery endothelial cell) lysates to pre-formed HOSCN, or MPO/H2O2/Cl(-) with increasing SCN(-), increased eNOS monomerization and Zn(2+) release, and decreased activity. Intact HCAECs exposed to HOCl and HOSCN had decreased eNOS activity and NO2(-)/NO3(-) formation (products of NO• decomposition), and increased free Zn(2+). Exposure of isolated rat aortic rings to HOSCN resulted in thiol loss, and decreased eNOS activity and cGMP levels. Overall these data indicate that high SCN(-) levels, as seen in smokers, can increase HOSCN formation and enhance eNOS dysfunction in human endothelial cells, with this potentially contributing to increased atherogenesis in smokers.