Tea catechins, (-)-epigallocatechin-3-gallate (EGCg) and (-)-epigallocatechin (EGC), have been reported to suppress oxidation of plasma low density lipoprotein (LDL) in vitro. If dietary catechins can be efficiently incorporated into human blood plasma, anti-atherosclerotic effects in preventing oxidative modification of LDL would be expected. In this study, a newly developed chemiluminescence detection-high pressure liquid chromatography (CL-HPLC) method for measuring plasma catechins was used and the incorporation of EGCg and EGC into human plasma was investigated. Healthy subjects orally ingested 3, 5, or 7 capsules of green tea extract (corresponding to 225, 375, and 525 mg EGCg and 7.5, 12.5, and 17.5 mg EGC, respective]y). The plasma EGCg and EGC concentrations before the administration were all below the detection limit ( < 2 pmol/ml), but 90 min after, significantly and dose-dependently increased to 657, 4300, and 4410pmol EGCg/ml, and 35, 144, and 255pmol EGC/ml, in the subjects who received 3,5, and 7 capsules, respectively. Both EGCg and EGC levels detected in plasma corresponded to 0.2-2.0·Yo of the ingested amount. Catechin intake had no effect on the basal level of endogenous antioxidants «(X-tocopherol, p-carotene, and lycopene) or of lipids in plasma. These results suggested that drinking green tea daily would contribute to maintain plasma catechin levels sufficient to exert antioxidant activity against oxidative modification of lipoproteins in blood circulation systems.

Both Colletotrichum and Magnaporthe spp. develop appressoria pigmented with melanin, which is essential for fungal pathogenicity. 1,8-Dihydroxynaphthalene (1,8-DHN) is believed to be polymerized to yield melanin around the appresorial cell wall through the oxidative activity of laccases. However, no 1,8-DHN laccase has yet been identified in either Colletotrichum or Magnaporthe spp. Here, we report a laccase gene, LAC2, that is involved in the appressorial melanization of Colletotrichum orbiculare, which causes cucumber anthracnose. LAC2 encodes a protein with a signal peptide and has high homology to fungal laccases. The conidial color of lac2 mutants is distinct from that of the C. orbiculare wild type, and the mutants are nonpathogenic. Notably, the mutant appressoria are defective in melanization, and a host invasion assay showed that the appressoria are nonfunctional. LAC2 was induced during appressorial melanization. These results suggest that LAC2 oxidizes 1,8-DHN in the appressoria. The LAC2 homologues of other fungi located in the same phylogenetic clade as LAC2 fully complemented the lac2 mutants. Interestingly, a LAC2 homologue, located in a different clade, complemented the conidial pigmentation but not appressorial melanization of the mutants, suggesting that the LAC2 function in appressorial melanization might only be conserved in laccases of the LAC2 clade.

Glucocorticoids have been widely used in the treatment of autoimmune and other diseases. Chronic steroid use, however, could cause proximal muscle weakness and atrophy, termed steroid myopathy. The onset of steroid myopathy is usually insidious and there are no specific laboratory findings except for elevated urinary creatine excretion. Muscle biopsy reveals non-specific type II fiber atrophy. There are many reports showing preventive effects of either growth hormone (GH) or insulin-like growth factor (IGF)-I on steroid myopathy. The pathogenesis of steroid myopathy is not fully understood. Recently, glutamine synthetase has been reported to play a key role in steroid myopathy. GH as well as IGF-I decreased the steroid-induced glutamine synthetase activity in skeletal muscle.

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We examined the effects of simultaneous administration of recombinant insulinlike growth factor-I (IGF-I) and glucocorticoid on the diameter of muscle fibers in rats. The steroid group received subcutaneous injection of triamcinolone, the IGF-treated group received IGF-I alone, and the steroid plus IGF group received both triamcinolone and IGF-I. After 14 days, each rat was subjected to muscle biopsy of the extensor digitorum longus and soleus. Glucocorticoid treatment caused significant reduction in diameter of muscle fibers, compared to controls. Simultaneous administration of IGF-I significantly attenuated glucocorticoid-induced muscle atrophy. Glucocorticoid increased both urinary concentration of 3-methylhistidine and urinary creatine/creatinine ratio. IGF-I reduced those changes in the urine. We conclude that IGF-I administration prevents, at least partially, the development of steroid myopathy. A well-known side effect of prolonged glucocorticoid treatment is the muscle atrophy and weakness known as steroid myopathy.2 We previously demonstrated the preventive effect of recombinant human growth hormone (GH) on experimental steroid myopathy in rats. 23 Numerous other reports have indicated the anabolic effects of GH on skeletal muscle. 7,13,16,21,34,36 Because muscle cells possess their own receptors for GH, 1 GH possibly exerts a direct anabolic action on skeletal muscle. 13,16,26,34