Influence of the habitat altitude on the (proto)hypericin and (proto)pseudohypericin levels of hypericum plants from Crete.

Environmental factors are known to influence strongly the accumulation of secondary metabolites in plant tissues. In a previous paper, we studied the contents of (pseudo)hypericin and its immediate precursors in wild populations of various HYPERICUM species on the island of Crete, Greece, in dependence on their developmental stage. In this study, we investigated the effect of the habitat altitude on the total hypericins content of the plants, which is defined as the sum of protohypericin, hypericin, protopseudohypericin and pseudohypericin. Taking into account our previous finding that the highest accumulation is found during the flowering period in June, we collected the aerial parts of spontaneously growing H. PERFORATUM L. , H. TRIQUENTRIFOLIUM Turra , H. EMPETRIFOLIUM Willd. and H. PERFOLIATUM L. during that time frame at elevations between 100 and 600 m above sea level, however, bearing in mind the time lag in development with increasing altitude. HPLC analysis of the plant material, separated again into a flowers and a leaves/petioles fraction, revealed great differences in the total hypericin content in dependence on the altitude of the habitat. Specifically, a clear trend was revealed, showing an increase of the total hypericin content with increasing altitude. However, no changes could be observed in the ratio of hypericin to protohypericin and in that of pseudohypericin to protopseudohypericin. The habitats of the employed plants were again randomly distributed all over Crete. It is proposed that higher light intensities accompanied by enhanced UV-B radiation and lower air temperature might be responsible for the increasing levels of total hypericins with increasing altitude

PTERIN- AND FLAVIN-LIKE FLUORESCENCE ASSOCIATED WITH ISOLATED FLAGELLA OF Euglena gracilis.

Fluorescence excitation- and emission spectra indicate the presence of pterin(s) and flavin(s) in isolated flagella of the phytoflagellate Euglena gracilis. These compounds appear to bind at least in part non-covalently to the molecular framework of the paraflagellar body, which is the presumed photoreceptor organelle and which is attached to the isolated flagella. A compound with pterin-like fluorescence excitation and emission spectrum could he extracted with methanol from isolated flagella and could he recovered on thin-layer silica gels. Besides the previously assumed photoreceptor function of flavins, our results suggest also a role for pterins in the photosensory transduction chain of Euglena gracilis.

Is 5-aminolevulinic acid involved in the hepatocellular carcinogenesis of acute intermittent porphyria?

5-Aminolevulinic acid (ALA) is a heme precursor that accumulates in acute intermittent porphyria (AIP) due to enzymatic deficiencies in the heme biosynthetic pathway Its accumulation has been associated with several symptoms, such as abdominal pain attacks, neuromuscular weaknesses, neuropsychiatric alterations and increased hepatocellular carcinoma (HCC) incidence. The use of exogenous ALA to elevate porphyrin levels in tumor photodynamic therapy, adds further significance to ALA toxicology. Under ferritin mediated and metal catalyzed oxidation, ALA produces reactive oxygen species that can damage plasmid and isolated DNA in vitro, and increases the steady-state level of 8-oxo-7,8-dihydro-2'-deoxyguanosine in liver, spleen and kidney DNA and 5-hydroxy-2'-deoxycytidine in liver DNA of ALA-treated rats. The in vitro DNA damage could be partially inhibited by SOD, catalase, DTPA, mannitol and melatonin. ALA also promotes the formation of radical-induced base degradation products in isolated DNA. 4,5-Dioxovaleric acid, the final oxidation product of ALA, alkylates guanine moieties within both nucleoside and isolated DNA, producing two diastereoisomeric adducts. Dihydropyrazine derivatives of ALA generated by its dimerization, promote DNA strand-breaks and 8-oxodGuo formation in the presence of Cu2+. Together these results reinforce the hypothesis that the DNA damage induced by ALA may be associated with the development of HCC in individuals suffering from AIP.