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Lentinus edodes (Shiitake) is a medicinal mushroom with a long tradition of use in Asia. The major active substance in L. edodes is a (1-6,1-3)-beta-glucan (lentinan). No clinical controlled studies have yet investigated the effect of orally administered lentinan on the immune response in healthy, elderly Caucasian subjects. We evaluated the effect and the safety of a beta-glucan from L. edodes mycelium, Lentinex, in healthy, elderly subjects in a double blind, crossover, placebo-controlled trial. Forty-two subjects were randomly allocated to two groups given orally either 2.5 mg/day Lentinex or placebo for 6 weeks; then after a washout period of 4 weeks, the alternate supplementation was given for 6 weeks. The changes in the number of B-cells were significantly different between the groups. The number ofNK cells increased significantly in both groups, but there was no significant difference between the groups. Other factors of the immune response (immunoglobulins, complement proteins, cytokines) were not altered. The safety blood variables (differential cell count, liver function, kidney function, and other blood chemistry) were not influenced by Lentinex, and the number, nature, and severity of adverse events were similar to placebo. Lentinex given orally to elderly subjects was safe and induced an increase in the number of circulating B-cells.

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1. We investigated the nature and roles of various xenobiotic acyl-CoA hydrolases in liver subcellular fractions from rat treated with sulphur-substituted (thia) fatty acids. To contribute to our understanding of factors influencing enzymes involved in the degradation of activated fatty acids, the effects on these activities of the oppositely acting thia fatty acid analogues, the peroxisome proliferating 3-thia fatty acids (tetradecylthioacetic acid and 3-dithiacarboxylic acid), which are blocked for beta-oxidation, and a non-peroxisome-proliferating 4-thia fatty acid (tetradecylthiopropionic acid), which undergoes one cycle of beta-oxidation, were studied. 2. The hepatic subcellular distributions of palmitoyl-CoA, tetradecylthioacetyl-CoA and tetradecylthiopropionyl-CoA hydrolase activities were similar to each other in the control and 3-thia fatty acid-treated rat. In control animals, most of these hydrolases were located in the microsomal fraction, but after treatment with the 3-thia fatty acids, the specific activities of the mitochondrial, peroxisomal, and cytosolic palmitoyl-CoA, tetradecylthioacetyl-CoA, and tetradecylthiopropionyl-CoA hydrolase activities were significantly increased. This increase in activity was seen mostly for the enzymes using tetradecylthiopropionyl-CoA and tetradecylthioacetyl-CoA as substrates. The increased mitochondrial activities for these two substrates were seen already after 1 day of treatment, whereas the peroxisomal activities increased after 3 days. No stimulation was seen after treatment with the 4-thia fatty acid analogue, tetradecylthiopropionic acid, but a decrease in peroxisomal hydrolase activities for all three substrates was observed. 3. The cellular distributions of clofibroyl-CoA, POCA-CoA, and sebacoyl-CoA hydrolase activities were different from those of the 'long-chain acyl-CoA' hydrolases mentioned above both in the normal and 3-thia fatty acid treated rat. This group of hydrolases was found in the mitochondrial, peroxisomal, and cytosolic fractions. 3-Thia fatty acid treatment increased the activities of clofibroyl-CoA and sebacoyl-CoA hydrolases in all three fractions. Clofibroyl-CoA and sebacoyl-CoA hydrolase activities were increased after 1 day of treatment. Only the cytosolic POCA-CoA hydrolase was stimulated after 3-thia fatty acid treatment after only 1 day of treatment, whereas treatment with the 4-thia fatty acid led to an increase of enzyme activity in the mitochondrial and peroxisomal fractions. 4. Based on the subcellular distributions and specific activities, we suggest that several enzymes exist which may act as regulators of intracellular acyl-CoA levels.

The rate of oxidation of fatty acids in mammals is minimal prior to birth. In this study, we have shown that foetal calf serum (FCS) inhibits oxidation of palmitate while serum from newborn calves is almost without effect. Foetal calf serum was also found to increase fatty acid synthesis from acetate. Uptake of laurate in mitochondria is partially dependent upon the carnitine palmitoyltransferase (CPT) I/CPT II system, while octanoate transport occurs without its participation. Comparison of the effects of FCS on the oxidation of palmitate, laurate and octanoate supports the view that the observed actions of FCS result from regulation of CPT I activity. The material in FCS that affects fatty acid metabolism has a molecular weight <3 kDa, as determined by dialysis and ultra-filtration studies.

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