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EN
Background The aim of the study was to evaluate serum levels of the target enzyme for H2S toxicity – cytochrome c oxidase (COX) and enzymes involved in the synthesis of H₂S – cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE) in copper mine miners. Material and Methods The initial and basic study was conducted respectively in 237 and 88 miners, working in 2 mining shafts: I – no H₂S emissions recorded in the last 10 years (study group A) and II – H₂S emissions occurred (study group B). A medical examination was performed and 10 ml of blood was collected from miners immediately after exiting the mine. Results There were no clinical or biochemical changes typical for H₂S toxicity. Sulfhemoglobine was undetectable and there were no changes in the red-ox system. However, in group B, regulatory changes were found; a tendency to higher concentration of CBS and CSE, a higher activity of angiotensin converting enzyme (ACE) compared to group A (p < 0.05) and a linear relationship between ACE and CSE (r = 0.6927; p < 0.001). It has been shown that cigarette smoking decreases COX (p < 0.05), however, in miners working in shaft II, the decreased level of COX may result also from the presence of H₂S in the gaseous emissions. Conclusions COX concentration can be a sensitive indicator of exposure to H₂S. The measurements of blood H₂S concentrations carried out in workplaces should explain the cause of the changes observed in the COX, CBS and CSE activity. Med Pr 2015;66(4):539–548
PL
Wstęp Celem badań była ocena stężenia mitochondrialnego enzymu docelowego dla toksycznego działania siarkowodoru, tj. oksydazy cytochromu c (COX) oraz enzymów uczestniczących w syntezie endogennego H₂S (siarkowodoru) – syntazy β-cystationiny (CBS) i γ-liazy cystationiny (CSE) w surowicy górników kopalni miedzi. Materiał i metody Badanie wstępne przeprowadzono u 237 górników, a zasadnicze u 88 górników zatrudnionych w 2 szybach: I – bez zarejestrowanych emisji H₂S w ciągu ostatnich 10 lat (grupa badana A); II – w którym występowały emisje H₂S (grupa badana B). U górników przeprowadzono badania lekarskie i bezpośrednio po wyjeździe z kopalni na powierzchnię pobrano od nich po 10 ml krwi żylnej. Wyniki Nie stwierdzono żadnych zmian klinicznych ani biochemicznych, typowych dla toksycznego działania siarkowodoru. Stężenie sulfhemoglobiny było nieoznaczalne, nie stwierdzono zmian w układzie oksydo-redukcyjnym. W grupie B wykazano natomiast zmiany regulacyjne, które mogą być wynikiem powtarzanych ekspozycji na H₂S. Do tych zmian należy wyższe stężenie CBS i CSE w surowicy, wzrost aktywności enzymu konwertującego angiotensynę (ACE) w porównaniu z grupą A oraz liniowa zależność między ACE a CSE (r = 0,6927; p < 0,001). Wykazano, że palenie papierosów obniża stężenie COX (p < 0,05), jednak u górników zatrudnionych w szybie II obniżenie stężenia COX może wynikać, poza paleniem, także z obecności siarkowodoru w gazach kopalnianych. Wnioski Stężenie COX może być czułym wskaźnikiem ekspozycji na siarkowodór. Pomiary stężenia siarkowodoru we krwi przeprowadzane na stanowiskach pracy powinny wyjaśnić przyczynę zmian w aktywności COX, CBS i CSE. Med. Pr. 2015;66(4):539–548
EN
ObjectivesWhile inorganic mercury is being gradually withdrawn from industry, environmental exposure to mercury is recognized as one of the greatest present toxicological problems. The aim of this study was to evaluate the effect of polyunsaturated fatty acids (PUFAs) supplementation on selected cardiovascular risk factors and the urinary mercury (Hg-U) concentration in workers occupationally exposed to mercury vapor.Material and MethodsOverall, 38 workers of an electrolyzer hall (Hg-U: 46.6±35.7 μg/g creatinine) and a control group of 60 employees not exposed to Hg (Hg-U: 4.3±15.5 μg/g creatinine) were included in a clinical cross-over study. Clinical and laboratory tests were carried out 4 times: before and after a 3-month period of PUFAs supplementation (1000 mg daily), then after a 3-month break, and then after another 3-month period of PUFAs supplementation.ResultsThe baseline heart rate (HR) and serum triglyceride levels were higher in the Hg-exposed workers than in the controls, whereas systolic blood pressure (SBP) and cholesterol (C) levels exceeded normal values in both groups. There was a positive correlation between high-density lipoprotein 3 cholesterol (HDL3-C) and Hg-U levels. The PUFAs use was associated with a decrease in both HR and SBP. After the first stage of supplementation, a decrease in the Hg-U concentration was observed. In a multivariate logistic regression model, decreases in Hg-U were associated only with exposure to mercury; ORΔHg = 0.562 (95% CI: 0.323–0.979), p < 0.042. After the second 3-month period of PUFAs supplementation, a significant association between HDL3-C and a Hg-U decrease was shown: OR HDL3 = 1.222 (95% CI: 1.01–1.46), p < 0.033.ConclusionsIn the workers exposed to mercury vapor, PUFAs supplementation led to some beneficial effects on HR and SBP. The first stage of supplementation was associated with a decrease in Hg-U in which HDL3 metabolism probably plays an important role.
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