Spectrofluorometric Analysis of Phylloerythrin in Plasma and Skin from Sheep Suffering from Hepatogenous Photosensitization

摘要

In hepatogenous photosensitization diseases, hepatic excretion of phylloerythrin is decreased or ceased causing retention of phylloerythrin (Flaoyen, 1999). Phylloerythrin is a metabolic product of chlorophyll produced in ruminants by rumen microorganisms (Rimington and Quin, 1933; Quin et al., 1935). Unlike chlorophyll, which has a long phytyl side chain preventing it from being absorbed from the digestive tract, phylloerythrin has lost the side chain and can be absorbed from the gut. Normally, phylloerythrin is conjugated by the liver and excreted into the bile, but some types of liver damage or liver dysfunction impair the hepatic elimination of phylloerythrin. Thus, phylloerythrin enters the bloodstream and reaches the skin cells where it accumulates intracellulary (Slater and Riley, 1966). Phylloerythrin is a porphyrin (Fischer and Kilmer, 1925) and has its absorption (about 420 nm) in the visible region. An acute inflammatory response of the skin is induced when phylloerythrin is excited by sunlight. Excitation initiates reactions that require molecular oxygen. Excited phylloerythrin molecules transfer their energy to oxygen, thus causing the formation of toxic singlet oxygen or oxygen radicals. Singlet oxygen is believed to be the main cytotoxic agent of porphyrin-like molecules (Weishaupt et al., 1976; Agarwal et al., 1992).