This study aimed to evaluate the reduction of total, organic, and inorganic arsenic content in Hizikia fusiforme (hijiki). Initially, the six most common arsenic compounds in hijiki and its organs were evaluated, among which only arsenate and arsenobetaine were detected. Thereafter, the entire plant, including the stalk and leaves, was treated with heat and NaCl solution, individually and in combination. Heating at 90 °C for 5 min significantly reduced arsenic content in hijiki by approximately 33-80%. Treatment with NaCl solution significantly reduced arsenic content in hijiki, except for arsenobetaine content in the stalk. Combinatorial treatment further decreased arsenic content by more than 5-20%. In conclusion, consumption of hijiki after boiling at 90 °C and soaking in 2% NaCl solution reduces the intake of inorganic arsenic by consumers.

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It was found from HPLC analysis that a commercial herb drink contains a putative sildenafil analog. In order to identify the sildenafil-like compound, separation and purification were carried out. The structure determination was performed based on routine 1D and 2D NMR experiments. Unlike sildenafil, the compound contains an ethylpiperazine instead of a methylpiperazine group. In addition, the piperazine and phenyl groups are connected through an acetyl group instead of the sulfonyl group of sildenafil.

In the course of screening for anticancer agents, a novel active compound, F3-2-5, was isolated from culture broth of Streptomyces sp., KACC91015. Its structure was identified using nuclear magnetic resonance, mass spectrometry, and molecular modeling experiments, and confirmed by total synthesis. The growth of various human cancer cell lines was inhibited in a dose-dependent manner by 0.06-0.48 mM F3-2-5 over 24 h. Its IC 50 values were estimated at 37 µ µ µ µM on HeLa, 72 µ µ µ µM on A549, and 190 µ µ µ µM on HT-29 cells. However, F3-2-5 had no antiproliferative effect on normal lymphocytes and normal fibroblasts used as controls. Moreover, it affected cell cycle regulation and caused apoptosis of the HeLa cells; chromatin condensation and DNA fragmentation were observed in cells exposed to 80 µ µ µ µM F3-2-5. Western blot analysis revealed that F3-2-5 inhibited phosphorylation of retinoblastoma protein (pRb) and reduced expression of cyclindependent kinase-4 and -6, and cyclin D1 and E, while levels of p53 and p21 WAF1/CIP1 increased. Taken O ver the last decade basic cancer research has achieved remarkable advances in the understanding of cancer biology and cancer genetics.(1) Although many anticancer drugs have been developed, most are also toxic to normal cells and tissues, and thus have limited selectivity for cancer cells. Therapeutic use has therefore been restricted to only a few drugs.(2) To overcome these limitations and improve the effectiveness of chemotherapy for cancer, it is necessary not only to isolate new anticancer drugs specifically toxic for cancer cells, but also to identify new targets that destroy cancers when exposed to chemotherapy.The cell cycle in eukaryotes is regulated by a precise balance between positive and negative regulatory components that exert their effects during the G 1 phase. The most critical positively acting components are G 1 cyclins (cyclin Ds and cyclin E) and CDK.(3-6) The G 1 -S transition is dependent on activation of G 1 phase CDK, and phosphorylation of pRb. (7,8) Cyclin D associates with CDK4 and CDK6, causing their activation, which in turn promotes progression through early G 1 phase.(5) Cyclin E and CDK2 proteins act at the transition from the G 1 to the S phase. The G 1 phase-specific cyclins and CDK complexes phosphorylate pRb and release it from its inhibitory association with the transcription factor E2F; the latter then promotes expression of S phase-specific genes. (7,8) In addition, cyclin A is produced in late G 1 phase, and expressed during the S and G 2 phases.(9) The activity of the CDK is inhibited by CKI, such as p21 WAF1/CIP1 and p27 KIP1 thereby blocking cell proliferation. (10)(11)(12)(13) In addition, cell cycle arrest dependent on the tumor suppressor p53 requires transactivation of p21 WAF1/CIP1 . (14) Inhibitors of cell cycle progression have potential as anticancer agents. (15)(16)(17) Apoptosis is also an important determinant of the response of tumors to chemotherapeutic agents.(18) The morphological features of apoptosis include c...