5-Aminolevulinic Acid HCl is an intermediate in the porphyrin synthesis pathway, used as a photosensitizing agent and a antineoplastic agent.
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5-Aminolevulinic Acid HCl is an intermediate in the porphyrin synthesis pathway, used as a photosensitizing agent and a antineoplastic agent. In vitro
5-aminolevulinic acid (5-ALA)-Photodynamic therapy (PDT) results in down regulation of nuclear factor kappa B (NFkappaB) and baculovirus inhibitor-of-apoptosis repeat containing-3 (BIRC-3) protein. 5-aminolevulinic acid (5-ALA)-Photodynamic therapy (PDT) causes increase in Bax:Bcl-2 ratio and mitochondrial release of cytochrome c and apoptosis-inducing factor (AIF). 5-aminolevulinic acid yields reactive oxygen species upon metal-catalyzed oxidation and causes in vivo and in vitro impairment of rat liver mitochondria and DNA damage. 5-aminolevulinic acid induces a dose-dependent damage in nuclear and mitochondrial DNA in human SVNF fibroblasts and rat PC12 cells. 5-aminolevulinic acid dose-dependently decreases cAMP levels (maximal inhibition of 38%, at 1 mM), due to an inhibition of basaladenylate cyclase activity. 5-aminolevulinic acid also inhibits fluoride- and Gpp(NH)p-stimulated, but not the forskolin-stimulated adenylate cyclase activity. 5-aminolevulinic acid also inhibits the activity of adenylate cyclase in membranes isolated from rat cortex and striatum and from human cortex. 5-aminolevulinic acid (0-3mM) dose-dependently inhibits glutamate uptake by astrocyte cultures. 5-aminolevulinic acid significantly reduces both the K(m) and V(max) of glutamate uptake indicating an uncompetitive inhibition. 5-aminolevulinic acid significantly increases astrocyte lipoperoxidation in astrocytes incubated under these conditions. 5-aminolevulinic acid mediated sonodynamic therapy exhibits synergistic apoptotic effects on THP-1 macrophages, involving excessive intracellular reactive oxygen species generation and MMP loss.
