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Curcumin, one of the most studied chemopreventive agents, is a natural compound extracted from Curcuma longa L. Extensive research over the last half century has revealed that curcumin can inhibit the proliferation of various tumor cells in culture, prevent carcinogen induced cancers in rodents and inhibit the growth of human tumors in xenotransplant or orthotransplant animal models. Several phase I and phase II clinical trials indicated that curcumin is quite safe and may exhibit therapeutic efficacy. The utility of curcumin is limited by its lack of water solubility and relatively low in vivo bioavailability. Multiple approaches including nanoparticles, liposomes, micelles and phospholipid complexes are being sought to overcome these limitations. This review describes the general properties of curcumin and its potential effect against cancer including evidences of its antitumor action in vitro, in vivo, clinically and the strategies to overcome its low bioavailability.

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Advanced glycation end products (AGEs) can stimulate osteoblast apoptosis and have a critical role in the pathophysiology of diabetic osteoporosis. Mitochondrial abnormalities are closely related to osteoblast dysfunction. However, it remains unclear whether mitochondrial abnormalities are involved in AGE-induced osteoblastic cell apoptosis. Silibinin, a major flavonolignan compound of silimarin, has strong antioxidant and mitochondria-protective properties. In the present study, we explored the possible mitochondrial mechanisms underlying AGE-induced apoptosis of osteoblastic cells and the effect of silibinin on osteoblastic cell apoptosis. We demonstrated that mitochondrial abnormalities largely contributed to AGE-induced apoptosis of osteoblastic cells, as evidenced by enhanced mitochondrial oxidative stress, conspicuous reduction in mitochondrial membrane potential and adenosine triphosphate production, abnormal mitochondrial morphology, and altered mitochondrial dynamics. These AGE-induced mitochondrial abnormalities were mainly mediated by the receptor of AGEs (RAGE). In addition, we found that silibinin directly downregulated the expression of RAGE and modulated RAGE-mediated mitochondrial pathways, thereby preventing AGE-induced apoptosis of osteoblastic cells. This study not only provides a new insight into the mitochondrial mechanisms underlying AGE-induced osteoblastic cell apoptosis, but also lays a foundation for the clinical use of silibinin for the prevention or treatment of diabetic osteoporosis.

Traditional processes usually cannot enable efficient water decontamination from toxic heavy metals complexed with organic ligands. Herein, we first reported the removal of Cu(II)−EDTA by a UV/chlorine process, where the Cu(II)−EDTA degradation obeyed autocatalytic two-stage kinetics, and Cu(II) was simultaneously removed as CuO precipitate. The scavenging experiments and EPR analysis indicated that Cl • accounted for the Cu(II)−EDTA degradation at diffusion-controlled rate (∼10 10 M −1 s −1 ). Mechanism study with mass spectrometry evidence of 11 key intermediates revealed that the Cu(II)−EDTA degradation by UV/chlorine was an autocatalytic successive decarboxylation process mediated by the Cu(II)/Cu(I) redox cycle. Under UV irradiation, Cu(I) was generated during the photolysis of the Cl • -attacked complexed Cu(II) via ligand-to-metal charge transfer (LMCT). Both free and organic ligand-complexed Cu(I) could form binary/ternary complexes with ClO − , which were oxidized back to Cu(II) via metal-to-ligand charge transfer (MLCT) with simultaneous production of Cl • , resulting in the autocatalytic effect on Cu(II)−EDTA removal. Effects of chlorine dosage and pH were examined, and the technological practicability was validated with authentic electroplating wastewater and other Cu(II)−organic complexes. This study shed light on a new mechanism of decomplexation by Cl • and broadened the applicability of the promising UV/chlorine process in water treatment.

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