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We characterized the biological functions of protocatechualdehyde (PA) isolated from the butanol extract of culture supernatant from Streptomyces lincolnensis M-20. Following butanol extraction, it was purified by silica gel and Sephadex LH-20 column chromatography. PA was analyzed by Furier Transform Infrared Spectroscopy (FT-IR), Gas chromatograph-Mass Spectrometer (GC-MS), and Nuclear Magnetic Resonance (NMR). PA had potent antioxidant activity, as measured by 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging activity. Antitumor activity against MCF-7 human breast cancer cells was evaluated by the 3-(4,5-dimethylthazol-2-yl)-2,5-diphenyl tetrazolium-bromide (MTT) assay. PA treatment (0 approximately 150 muM) dose-dependently blocked apoptosis, as shown by improved cell viability and inter-nucleosomal DNA fragmentation. Our findings suggest that Streptomyces lincolnensis M-20, a lincomycin producer, also produces protocatechualdehyde.

Purine nucleosides were chlorinated by the reaction of acyl chloride in DMF with MCPBA under mild conditions with moderate yields. And, satisfactory method for the synthesis of ribonucleoside-3',5'-cyclic phosphates and its characterization by(1)H and(13)C nmr spectroscopy is described.

From the freeze dried leaves ofAloe vera, aloe-emodin, feralolide, a mixture of aloins A and B, elgonica dimers A and B were isolated and characterized based on spectral data.

Effects of betaine on glutamate-induced neurotoxicity were examined on primary cultures of chicken embryonic brain cells and on rat cortical cultures. Betaine was found to attenuate glutamate-induced neurotoxicity both morphologically and biochemically. A 30 min exposure of chicken embryonic brain cells cultured for 12 days to 500 μM glutamate produced wide-spread acute neuronal swelling and neuritic fragmentation. A 2-h pretreatment of cultured chicken embryonic brain cells with 1 mM betaine prior to a 30 min exposure to 500 μM glutamate significantly raised the survival rate of neurons in the culture. When chicken embryonic brain cells were pretreated for 2 h with 1 mM betaine followed by exposure to 100 μM glutamate for 42 h, lactate dehydrogenase levels within the cells remained at 63% of untreated control values while glutamate-treated controls fell to 0% lactate dehydrogenase. Betaine also exerted attenuating effects on N-methyl-D-aspartate-, kainate- and quisqualate-induced neurotoxicity in a similar manner to that observed with glutamate. Similar neuroprotective effects of betaine were obtained with rat cortical cultures.