Stenac Mechanism of Action

Pharmacology: Pharmacodynamics Acetylcysteine is the main active composition in the effervescent tablets, through directly interaction with mucoprotein complex and nucleic acid then to disrupt the mucoprotein of phlegm into smaller clear units and thereby reduces the viscosity of the phlegm. Acetylcysteine as a mucolytic agent results from its sulfhydryl interacting with disulfide bonds in mucoprotein, with the mucus subsequently being broken into less viscous units.
Acetylcysteine, an antioxidant, with active free sulfahydryl group can interact with reactive oxygen species. Acetylcysteine have a therapeutic application in preventing oxidative tissue injury induced by hypochlorous acid (HOCl). HOCl is toxic to cells because it initiates oxidative injury and causes the activation of phagocyte peroxidases, such as the neutrophil enzyme MPO. Acetylcysteine has been shown to dramatically reduce the viscosity and tenacity of sputum. The liquefying action is due to the presence of a free sulphydryl group which opens up disulphide bonds present in mucus. Pretreatment with Acetylcysteine may prevent lung injury by diminishing elastase activity; this diminished activity of elastase may be achieved by enhanced inactivation by antiproteases.
It is concluded that acetylcysteine is useful for viscosity and maturative secretion of phlegm induced by acute and chronic respiratory system inflammation. In addition, the structure of acetylcysteine can transport through cell membrane and decompose to L-cysteine, the main component of glutathione (GSH), and maintains cellular GSH at a level. GSH, an antioxidant, protects cells from toxins such as free radicals.
Acetaminophen overdose: The primary toxic effect of acetaminophen is hepatotoxicity caused by the formation of the toxic metabolite N-acetyl-pbenzoquinonimine (NAPQI). NAPQI is conjugated by glutathione at therapeutic dosages. In an overdose, the normal pathways of metabolism are overwhelmed and NAPQI is formed in greater quantities, resulting in depletion of glutathione and hepatic injury. Administration of NAC is beneficial in preventing or mitigating hepatic injury through stimulation of glutathione synthesis, enhancing nontoxic routes of acetaminophen metabolism, detoxifying the toxic metabolite and free radical scavenging.
Pharmacokinetics: Acetylcysteine is rapidly absorbed from the gastrointestinal tract and peak plasma concentrations occur about 0.5 to 1 hour after oral doses of 200 to 600mg. Some studies indicate dose-dependent pharmacokinetics with peak concentrations, the time taken to reach peak concentrations, and bioavailability increasing with increasing doses.
Acetylcysteine may be present in plasma as the parent compound or as various oxidized metabolites such as N-acetylcystine, N,N-diacetylcystine, and cysteine either free or bound to plasma proteins by labile disulfide bonds or as a fraction incorporated into protein peptide chains. In a study about 50% was in a covalently protein-bound form 4 hours after a dose. Oral bioavailability is low and means values have ranged from 4 to 10% depending on whether total acetylcysteine or just the reduced forms are measured. It has been suggested that acetylcysteine's low oral bioavailability may be due to metabolism in the gut wall and first-pass metabolism in the liver. Renal clearance may account for about 30% of total body clearance. On intravenous dosage mean terminal half-lives have been calculated to be 1.95 and 5.58 hours for reduced and total acetylcysteine, respectively; the terminal half-life of total acetylcysteine was 6.25 hours after oral doses. Absorption of NAC is rapid following oral administration, but the bioavailability is only 6-10% due to extensive first-past metabolism. In addition, oral administration is often limited by nausea and vomiting which results in delayed or ineffective administration of NAC. Intravenous administration of NAC results in 100% bioavailability. The mean terminal half-life is approximately 6 hours. Clearance is not reduced and plasma concentrations are not increased in patients with severe liver damage. Currently there is no dosage adjustment recommended for patients with renal or hepatic insufficiency.