Abstract:
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. 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.
journal_name
Med Prjournal_title
Medycyna pracyauthors
Skoczyńska A,Gruszczyński L,Turczyn B,Ścieszka M,Wojakowska A,Pawłowski T,Schmidt Edoi
10.13075/mp.5893.00207subject
Has Abstractpub_date
2015-01-01 00:00:00pages
539-48issue
4eissn
0465-5893issn
2353-1339pii
58806journal_volume
66pub_type
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