UTICAJ DUGOTRAJNE PROŠLE EKSPOZICIJE ELEMENTARNOJ ŽIVI NA ANTIOKSIDATIVNI KAPACITET I LIPIDNU PEROKSIDACIJU U RUDARA ŽIVE
Kobal AB 1, Osredkar J. 2, Horvat M. 3, Prezelj M. 2, Sesek Briski A. 2, Krsnik M. 2, Dizdarević T. 1, Fajon V. 3, Gibicar D. 3, Falnoga I. 3, Stibilj V. 3, Arneric N. 4, Kobal D. 5
1 Idrija Mercury Mine, Idrija, Slovenia;
2 Institute of Clinical Chemistry and Biochemistry, University Medical Centre, Ljubljana, Slovenia;
3 Jožef Stefan Institute, Ljubljana, Slovenia;
4 Clinical Institute of Occupational, Traffic and Sports Medicine, University Medical Centre Ljubljana, Slovenija;
5 Department of Psychology, University of Ljubljana, Ljubljana, Slovenija;

Ograničene su raspoložive informacije o efektima hronične ekspozicije živi i rizicima za kardiovaskularna oboljenja s tim u vezi (CVD). Poznato je prema urađenim studijama in vitro i in vivo da Hg može poduprijeti lipidnu peroksidaciju preko aktiviracije formiranja slobodnih radikala. i interakcijom sa antioksidativnim enzimima i selenijumom.

CILJ: Cilj ove studije je testirati hipotezu da dugotrajna profesionalna ekspozicija elementarnoj Hg (Hg0) može mijenjati antioksidativni kapacitet i poduprijeti nastanak lipidne peroksidacije u rudara.

ISPITANICI I METODE: Populaciju istraživanja činilo je 54 rudara žive i 58 radnika koji su činili kontrolnu grupu. Rudari su ispitivani u periodu poslije ekspozicije. Mi smo pratili njihovu prethodnu ekspoziciju Hg0, navedene pojave nespecifičnih simptoma i znaka micromerkurializma, kao i glavne poremećaje ponašanja i biološke riziko faktore za CVD, uz određenja: (1) Hg i selenium (Se) nivoa u krvi i urinu, (2) Cu, Zn superoxide dismutase (CuZn-SOD), katalaze (CAT), selenoenzimske glutathionske peroxydazne (GSH-Px) aktivnosti u eritrocitima, hormona melatonina u krvi i urinu koji indirektno pokreće aktivaciju slobodnih radikala, (3) lipidnu hidroperoksidazu (LOOHs) i malondialdehyde (MDA) kao produkte lipidne peroksidacije.

REZULTATI: Rudari žive su povremeno bili izloženi Hg0 u trajanju od 7 do 31 godinu. Ukupan period izloženosti varira od 13 do 119. Kumulativni index U-Hg varirao je od 794-11365 µg/L. Koncentracije Hg u krvi i urinu bile su praktično istih vrijednosti u rudara i u kontrolnih ispitanika. Rudari su pokazivali neke neurotoksične i nefrotoksične posljedice mikromerkurializma. Nisu postojale signifikantne razlike u bihevioralnim i biološkim rizicima za CVD, otkriveni u rudara i kontrolnoj skupini. Otkrivena je slaba korelacija (r=0.36, P<0.01) između vrijednosti krvnog pritiska i srednjih vrijednosti nivoa prošle ekspozicije U-Hg. Srednje vrijednosti P-Se u rudara (71.4 µg/L) su bile signifikantno niže (P<0.05) nego u kontrolnih radnika (77.3 µg/L), dok su srednje vrijednosti U-Se imale rastuću tendencu (P<0.05) u rudara (16.5 µg/g creatinine) u odnosu na kontrolne subjekte (14.0 µg/g creatinine). Među antioksidativnim enzimskim aktivnostima, samo CAT u eritrocitima je bila signifikantno veća (P<0.01) u rudara (3.14 MU/g Hb) nego u kontrolnih subjekata (2.65 MU/g Hb). Srednje koncentracije B-melatonina u rudara (44.3 ng/L) su bile signifikantno veće (P<0.01) nego u kontrolnih ispitanika (14.9 ng/L). Srednja vrijednosti U-melatonin sulphata (31.8 µg/L) u rudara su bile signifikantno niže (P<0.01) u odnosu na kontrolnu grupu (46.9 µg/L). Observirani produkti lipidne peroksidacije, srednje vrijednosti U-MDA su bile statistički značajno više (P<0.01) u rudara (0.21 µmol/mmol kreatinina) u odnosu na kontrolnu grupu (0.17 µmol/mmol kreatinina).

ZAKLJUČCI: Rezultati ove studije potpomažu procjenu da dugotrajna profesionalna ekspozicija Hg0 povećava formiranje slobodnih radikala čak i nekoliko godina poslije terminalne profesionalne ekspozicije. Stoga je ekspozicija živi jedan od riziko faktora u rastućoj lipidnoj peroksidaciji i rastućem mortalitetu od ishemijskih oboljenja srca među rudarima rudnika žive Idrija .

THE IMPACT OF LONG-TERM PAST EXPOSURE TO ELEMENTAL MERCURY ON ANTIOXIDATIVE CAPACITY AND LIPID PEROXIDATION IN MERCURY MINERS
Kobal AB 1, Osredkar J. 2, Horvat M. 3, Prezelj M. 2, Sesek Briski A. 2, Krsnik M. 2, Dizdarević T. 1, Fajon V. 3, Gibicar D. 3, Falnoga I. 3, Stibilj V. 3, Arneric N. 4, Kobal D. 5
1 Idrija Mercury Mine, Idrija, Slovenia;
2 Institute of Clinical Chemistry and Biochemistry, University Medical Centre, Ljubljana, Slovenia;
3 Jožef Stefan Institute, Ljubljana, Slovenia;
4 Clinical Institute of Occupational, Traffic and Sports Medicine, University Medical Centre Ljubljana, Slovenija;
5 Department of Psychology, University of Ljubljana, Ljubljana, Slovenija;

Limited information is available on the effects of chronic mercury (Hg) exposure and the risk of cardiovascular disease (CVD). It is known from in vitro and in vivo studies that Hg can promote lipid peroxidation through the promotion of free radical generation, and interaction with antioxidative enzymes and selenium.

AIM: The objective of the study was to test the hypothesis that long-term past occupational exposure to elemental Hg (Hg0) can modify antioxidative capacity and promote lipid peroxidation in miners.

SUBJECTS AND METHODS:The study population comprised 54 mercury miners and 58 workers as the control group. The miners were examined in the post-exposure period. We evaluated their previous exposure to Hg0, the putative appearance of certain nonspecific symptoms and signs of micromercurialism, as well as the main behavioural and biological risk factors for CVD, and determined: (1) Hg and selenium (Se) levels in blood and urine, (2) Cu, Zn superoxide dismutase (CuZn-SOD), catalase (CAT), selenoenzyme glutathione peroxydase (GSH-Px) activity in erythrocytes, pineal hormone melatonine in blood and urine as indirect indices of free radical activity, (3) lipid hydroperoxides (LOOHs) and malondialdehyde (MDA) as lipid peroxidation products.

RESULTS: The mercury miners were intermittently exposed to Hg0 for periods of 7 to 31 years. The total number of exposure periods varied from 13 to 119. The cumulative U-Hg peak level varied from 794-11365 µg/L. The blood and urine Hg concentrations were practically on the same level in miners and controls. Miners showed some neurotoxic and nephrotoxic sequels of micromercurialism. No significant differences in behavioral and biological risk factors for CVD were found between miners and controls. A weak correlation (r=0.36, P<0.01) between systolic blood pressure and average of past expsoure U-Hg level was found. The mean P-Se in miners (71.4 µg/L) was significantly lower (P<0.05) than in the controls (77.3 µg/L), while the mean U-Se tended to be higher (P<0.05) in miners (16.5 µg/g creatinine) than in the controls (14.0 µg/g creatinine). Among antioxidative enzyme activities, only CAT in erythrocytes was significantly higher (p<0.01) in miners (3.14 MU/g Hb) than in the controls (2.65 MU/g Hb). The mean concentration of B-melatonine in miners (44.3 ng/L) was significantly higher (P<0.01) than in the controls (14.9 ng/L). The mean value of U-melatonine sulphate (31.8 µg/L) in miners was significantly lower (P<0.01) than in the control group (46.9 µg/L). Among the observed lipid peroxidative products, the mean concentration of U-MDA was statistically higher (P<0.01) in miners (0.21 µmol/mmol creatinine) than in the controls (0.17 µmol/mmol creatinine). CONCLUSUION: The results of our study support the assumption that long-term occupational exposure to Hg0 enhances the formation of free radicals even several years after termination of occupational exposure. And therefore could be one of the risk factors for increased lipid peroxidation and increased mortality due to ischaemic heart disease obtained among the mercury miners of the Idrija Mine.

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