[Mechanism of quenching of hematoporphyrin and mono-L-aspartyl chlorine e6 triplet states by metronidazole]. / O mekhanizme tusheniia tripletno-vozbuzhdennogo sostoianiia gematoporphirina i mono-L-aspartil khlorina e6 metronidazonom.

The quenching of the triplet state of hematopophyrin (3HP.) and mono-L-aspartyl chlorine e6, (3MACE.) by metrotlidazole (METRO) ground state, has been investigated in binary mixtures of water and aliphatic alcohol by means of 532 nm laser flash. In water, both 3HP. and 3MACE. quenched by METRO with at rate: kQw = 1.9 x 10(9) M-1.s-1. The quenching is accompanied by the appearance of a transient absorbance near 690 nm. This transient absorbance corresponds to the tetrapyrrole radical-cation formation in result of an electron transfer between 3HP. or 3MACE. and METRO. In neat alcohol, the electron transfer was not observed. In binary mixtures the quenching constant is reduced as the molar fraction of water is decreased. In water, the activation barrier of the quenching is 5.9 kcal/mol for HP and 3.9 kcal/mol for MACE. In going from water to water-alcohol mixtures the energy of activation is practically unchanged. Based on flash photolysis data, and analysis of absorption spectra of METRO we conclude that the electron-acceptor ability of metronidazole essentially depends on the intermolecular interaction with nearby solvent molecules. The mechanism of the quenching is discussed.

Degradation of crystallins from a psoriatic patient undergoing PUVA therapy.

Comparative physico-chemical and spectroscopic analyses were carried out in human lens proteins obtained from extracts of normal, senile and PUVA cataracts. Mass recovery analysis reveals a large protein concentration loss in the PUVA cataract relative to the normal lens and senile cataract. This protein loss parallels an increase in the degraded polypeptide chains. However, the tryptophan content (2.1 mol/mol of 20 kDa protein subunit) and the apparent fluorescence quantum yield (phi f = 0.056) of the tryptophan residues which are believed to be involved in the development of UV-induced cataracts are unchanged after age-related alterations and/or in vivo photochemistry associated with psoralen (8MOP) photosensitized reactions.