TALOŽENJE METALA (I METALOIDA) U SRČANOM TKIVU I MEHANIZMI KOJI LEŽE U OSNOVI NJIHOVIH KARDIOTOKSIČNIH EFEKATA
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Sažetak
Teški metali imaju snažan kardiotoksični efekat, a kardiomiociti su uopšteno govoreći osetljive ćelije, te su stoga veoma podložne toksičnosti uzrokovanoj prisustvom teških metala. Veza između izloženosti teškim metalima i njihovog doprinosa u patofiziologiji različitih kardiovaskularnih poremećaja, kao što su koronarna bolest srca (engl. coronary artery disease; CAD) i kardiomiopatije (engl. Cardiomyophaties; CMP), prepoznata je pretežno putem kliničkih istraživanja u kojima su nivoi metala ili metaloida mereni u krvi ili urinu osoba koje su imale pomenuta oboljenja. Međutim, ključna karika koja bi doprinela boljem razumevanju povezanosti teških metala i nastanku kardioloških oboljenja su studije koje ispituju taloženje teških metala unutar srčanog tkiva. Ovakve studije, bilo da su analizirani uzorci dobijeni post-mortem ili tokom invazivnih procedura u pacijenata, trenutno nedostaju. Kako bi se postiglo sveobuhvatno razumevanje potencijalne uloge metala i metaloida u nastanku CMP ili CAD, ovakva istraživanja su neophodna. Osim toga, određeni komorbiditeti kao što je nedostatak gvožđa mogu ubrzati taloženje teških metala u srčanom mišiću, povećavanjem gustine receptora za transferin (transferrin receptor 1; TfR1). Uticaj teških metala na kontraktilni aparat srca, zajedno sa njihovim potencijalom da započnu mitohondrijalnu apoptozu, čini deo složenog patofiziološkog pejzaža. Bazični mehanizmi uključeni u oštećenja usled prisustva teških metala su generisanje reaktivnih vrsta kiseonika (engl. Reactive oxygen species; ROS) i peroksidacija makromolekula.
U ovom članku ćemo se osvrnuti na studije koje su analizirale taloženje teških metala unutar miokarda; kao i na studije koje su se bavile molekularnim mehanizmima putem kojih metali ili metaloidi izazivaju kardiotoksičnost.
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