The ability of N-methyl mesoporphyrin IX (NMMP) to block heme synthesis by specificaly inhibiting enzymic iron insertion into protoporphyrin IX was exploited to test whether heme is a precursor of the biHn chromophore of phycocyanin (PC). A strain of the unicellular rhodophyte Cyanidiwn cadbiwm which forms normal amounts of both chorophyll (Chi) Biliproteins are the major light-harvesting pigments in bluegreen, red, and cryptomonad algae. The biliproteins are composed of open-chain phycobilin chromophore molecules which are covalently bound to proteins. Although the pigments are present in high abundance in the organisms in which they occur, their biosynthesis is poorly understood. Structural considerations suggest that phycobilins arise from macrocycle ring-opening of a porphyrin or metalloporphyrin precursor, but the relevant enzymic steps have not been observed in vitro (Fig. 1).Recently, Brown et al. (5) reported that exogenous '4C-heme was incorporated into phycocyanobilin, the bilin chromophore of PC2, but not into Chl, in greening cultures of the unicellular rhodophyte Cyanidium caldarium. This result suggests that heme is a metabolic precursor to the phycobilins. Others have proposed that the phycobilins might arise from the Mg-porphyrin branch of the tetrapyrrole pathway leading to Chl (1, 9). Possible biosynthetic paths to phycobilins are illustrated in Figure 2.
Diets higher in carbohydrate, fat or protein (diets 1, 2, and 3, respectively) were formulated isoenergetically with or without ethanol to study their effects on the accumulation of hepatic total lipids in rats fed for a period of 8 weeks. Ethanol ingestion did not affect body weight gain of rats fed diet 1, but diets 2 and 3 resulted in decreased weight gain as compared to the pair-fed controls. These body weight changes between control and ethanol groups were significant 2 weeks after beginning the treatment. Ethanol administration did not change hepatic weights of rats fed diet 1, but increased hepatic weights of rats fed diets 2 and 3. Higher protein alone in the diet increased liver weight. Ethanol intake increased the hepatic total lipid content of rats fed diets 2 and 3, but did not affect those fed diet 1 compared to their pair-fed controls. Hepatic cholesterol content increased in rats fed both the higher protein and higher fat diets. Both weight gain, liver weight, and hepatic total lipids consistently showed that the rats consuming 39% wheat starch as carbohydrate were not adversely affected by ethanol ingestion while those groups fed higher fat or higher protein with ethanol were adversely affected. Possible mechanisms are discussed.
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