In our cells, NAC is converted to cysteine which is a precursor of glutathione.The exact mechanism of how NAC prevents CIN has not been fully elucidated, however the theory is that it minimizes vasoconstriction and oxidative stress.In addition to antioxidant benefits, It may also be used as a mucolytic.NAC contains a free sulfhydryl group that may open disulfide bonds in mucoproteins. It is useful in an overdose because essentially what we are doing when we administer NAC is giving exogenous glutathione.However, in an overdose situation, the amount of APAP is high enough to overwhelm the primary route and its metabolism is shunted to the CYP system which increases the production of NAPQI, however because of the sharp increase, our glutathione stores also become overwhelmed and the end result is excess NAPQI that may covalently bind to hepatocytes and cause hepatic necrosis. From there, NAPQI is quickly converted to mercapturic acid by glutathione and is excreted in the urine.
The secondary route involves the CYP 450 system which converts APAP to a highly reactive oxide called NAPQI. Before I go over the mechanism of action, I thought I should explain the reason why NAC is useful as an antidote.APAP has 2 routes of metabolism, the primary route is through glucoronidation or sulphation which would make APAP more water soluble so that it may then be excreted in the urine.It is FDA approved as an antidote for APAP overdose, as adjunctive therapy for respiratory conditions, and as a mucolytic for diagnostic bronchial studies.The off-label uses are for the prevention of contrast-induced nephropathy and asAn adjunct in the treatment of H.NAC is a derivative of the amino acid cysteine.It is classified as a mucolytic and an antidote.
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