Disease relevance of N-Acetylpenicillamine

• Protective effects were not seen in traumatic shock rats treated with the non-NO-donating parent compound N-acetylpenicillamine [1].
• The administration of N-acetyl-DL-penicillamine 24 h after 63Ni injection increased significantly the urinary excretion of the metal and restored proteinuria during the next 24 h [2].
• Mercury poisoning in children. The value of N-acetyl-D,L-penicillamine in a combined therapeutic approach [3].
• Upon simultaneous administration of the same dose of N-acetylpenicillamine and 2,5 mmol/kg body weight of S-methylcysteine biliary excretion of methyl mercury increased only 1.5 fold [4].

High impact information on N-Acetylpenicillamine

• Both kinetics of the reaction and the mechanistic aspects of the decomposition of S-nitroso derivatives of glutathione, L-cysteine, N-acetyl-L-cysteine, N-acetyl-D,L-penicillamine, N-acetylcysteamine, L-cysteine methyl ester, and D,L-penicillamine have been investigated at neutral and acidic pH [5].
• A mechanism was proposed involving the hydrolysis of SNAP by an out of plane liganded H(2)O yielding the sulfenic acid of N-acetylpenicillamine and the transfer of NO(-) to Fe(III) [6].
• Formation constants for thallium(I) complexes of L-cysteine (CysH2), DL-penicillamine (PenH2), N-acetyl-L-cysteine (AcyH2), and N-acetyl-DL-penicillamine (ApeH2) in aqueous solution have been determined in 150 mmol dm-3 NaCl medium at 37 degrees C by potentiometric titrations using a glass electrode [7].
• Contrary, the antioxidative properties of N-acetylcysteine increased with its levels growing in the reaction mixture, and only N-acetylpenicillamine did not protect erythrocytes against oxidative damages [8].
• Treatment with SNAP (but not with N-acetylpenicillamine or SNAP + hemoglobin) not only induced apoptosis but resulted in a marked increase in p53 expression in cardiac myocytes detected by Western blotting and immunohistochemistry [9].

Associations of N-Acetylpenicillamine with other chemical compounds

• The compounds examined were N-Acetyl-D,L-penicillamine (NAPA), D-penicillamine (DPA), 2,3-dimercaptosuccinic acid (DMSA), sodium 2,3-dimercaptopropanesulfonate (DMPS), and 2,3-dimercaptopropanol-1 (BAL) [10].
• The protective effect of garlic was superior to those of 2,3 dimercapto-1-propanol (BAL) and D-penicillamine (PEN), and nearly similar to those of 2,3-dimercaptosuccinic acid (DMSA) and N-acetyl-DL-penicillamine (APEN), the current remedies, while garlic was not effective as a curative agent for heavy metal poisoning [11].
• The formation, reaction dynamics, and detailed kinetics and mechanism of the reaction between nitrous acid and N-acetylpenicillamine (NAP) to produce S-nitroso-N-acetylpenicillamine (SNAP) was studied in acidic medium [12].

Gene context of N-Acetylpenicillamine

• The effect of 1-chloro-2,4-dinitrobenzene (DNB), sulfobromophtalein (BSP) and cyclohexene oxide (cho) on N-acetylpenicillamine (NAPA) potentiated biliary excretion of methyl mercury in rats pretreated with cho for liver glutathione (GSH) depletion, has been tested [13].

Analytical, diagnostic and therapeutic context of N-Acetylpenicillamine

• Spontaneous degradation of SNAP and GSNO in tissue bathing medium (monitored by high-performance liquid chromatography) and the associated NO release (assessed by chemiluminescence detection of headspace NO) were enhanced in the presence of 100 microM N-acetylpenicillamine and inhibited in the presence of 100 U/ml superoxide dismutase [14].

References