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- Bd204bd312a4cd542a04f24c8babf6ab4 NCIT_P378 "NCI" @default.
- Bd204bd312a4cd542a04f24c8babf6ab4 type Axiom @default.
- Bd204bd312a4cd542a04f24c8babf6ab4 annotatedProperty IAO_0000115 @default.
- Bd204bd312a4cd542a04f24c8babf6ab4 annotatedSource NCIT_C200 @default.
- Bd204bd312a4cd542a04f24c8babf6ab4 annotatedTarget "A synthetic N-acetyl derivative and prodrug of the endogenous amino acid L-cysteine, a precursor of the antioxidant glutathione (GSH), with mucolytic, antioxidant, and potential cytoprotective, cancer-preventive, and anti-inflammatory activities. Upon administration, acetylcysteine exerts its mucolytic activity by reducing disulfide bonds in mucoproteins, resulting in liquification of mucus and reducing its viscosity. It is also used for the treatment of acetaminophen overdose as it can restore the depleted GSH reserves in the hepatocytes during the process of detoxification. The antioxidant activity is attributed to the ability of GSH to scavenge reactive oxygen species (ROS), thereby preventing ROS-mediated cell damage, decreasing oxidative stress, protecting cells against the damaging effects of free radicals and preventing apoptosis in these cells. In addition, this may inhibit tumor cell proliferation, progression and survival, in susceptible tumor cells that rely on ROS-mediated signaling for their proliferation and malignant behavior. Under certain circumstances, acetylcysteine is able to induce apoptosis in susceptible cells, including certain tumor cells, via the intrinsic mitochondria-dependent pathway but not involving endoplasmic reticulum stress. Also, acetylcysteine may also be able to degrade Notch2, thereby preventing proliferation, migration, and invasion in Notch2-overexpressing glioblastoma cells. In addition, acetylcysteine may inhibit viral stimulation by reactive oxygen intermediates, thereby producing antiviral activity in HIV patients. Acetylcysteine also possesses anti-inflammatory activity through modulation of the nuclear factor-kappa B (NF-kB) pathway and the modulation of cytokine synthesis." @default.