Yasoo Health Ltd

Nicosia, Cyprus

Yasoo Health Ltd

Nicosia, Cyprus

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Callion Health Llc and YASOO Health Inc. | Date: 2012-08-28

Pharmaceuticals in the nature of dietary iron supplements for medical use.


Constantinou C.,Yasoo Health Ltd. | Neophytou C.M.,University of Cyprus | Vraka P.,University of Cyprus | Hyatt J.A.,Yasoo Health Inc. | And 3 more authors.
Nutrition and Cancer | Year: 2012

Vitamin E comprises 8 functionally unique isoforms and may be a suitable candidate for the adjuvant treatment of prostate cancer. In this study, we examined the ability of 2 vitamin E isoforms [α-tocotrienol (γ-TT) and δ-tocotrienol (δ-TT)] and 4 synthetic derivatives [γ- and δ-tocotrienol succinate (γ-TS, δ-TS), α-tocopheryl polyethylene glycol succinate (TPGS), and -tocopheryl polyethylene glycol ether (TPGS-e)] of vitamin E to induce cell death in AR (DU145 and PC-3) and AR+ (LNCaP) prostate cancer cell lines. Our results show that δ-TT and TPGS-e are the most effective isoform and synthetic derivative, respectively, of all compounds examined. Overall, the results of our study suggest that isoforms and synthetic derivatives of vitamin E have the potency to trigger both caspase-dependent and -independent DNA damage and dominant caspase-independent programmed cell death. The capacity of vitamin E to trigger caspase-independent programmed cell death suggests that it may be useful in the chemotherapy of prostate cancer since it may prevent the tumor resistance commonly associated with the use of classical chemotherapeutic agents that trigger caspase-dependent programmed cell death. © 2012 Copyright Taylor and Francis Group, LLC.


Wells S.R.,LSUHSC S Molecular and Cellular Physiology | Jennings M.H.,LSUHSC S Molecular and Cellular Physiology | Rome C.,LSUHSC S Molecular and Cellular Physiology | Hadjivassiliou V.,Yasoo Health Ltd | And 2 more authors.
Journal of Nutritional Biochemistry | Year: 2010

Vitamin E, a micronutrient (comprising α-, β-, γ and δ-tocopherols, β-, γ and δ-tocotrienols), has documented antioxidant and non-antioxidant effects, some of which inhibit inflammation and angiogenesis. We compared the abilities of α-, γ- and δ-tocopherols to regulate human blood cytotoxicity (BEC) and lymphatic endothelial cytotoxicity (LEC), proliferation, invasiveness, permeability, capillary formation and suppression of TNF-α-induced VCAM-1 as in vitro models of inflammatory angiogenesis. α-, γ- and δ-tocopherols were not toxic to either cell type up to 40 μM. In BEC, confluent cell density was decreased by all concentrations of δ- and γ-tocopherol (10-40 μM) but not by α-tocopherol. LEC showed no change in cell density in response to tocopherols. δ-Tocopherol (40 μM), but not other isomers, decreased BEC invasiveness. In LEC, all doses of γ-tocopherol, as well as the highest dose of α-tocopherol (40 μM), decreased cell invasiveness. -Tocopherol had no effect on LEC invasiveness at any molarity. δ-Tocopherol dose dependently increased cell permeability at 48 h in BEC and LEC; α- and γ-tocopherols showed slight effects. Capillary tube formation was decreased by high dose (40 μM) concentrations of α-, γ- and δ-tocopherol, but showed no effects with smaller doses (10-20 μM) in BEC. γ-Tocopherol (10-20 μM) and α-tocopherol (10 μM), but not δ-tocopherol, increased LEC capillary tube formation. Lastly, in BEC, α-, γ- and δ-tocopherol each dose-dependently reduced TNF-α-induced expression of VCAM-1. In LEC, there was no significant change to TNF-α-induced VCAM-1 expression with any concentration of α-, γ- or δ-tocopherol. These data demonstrate that physiological levels (0-40 μM) of α-, γ- and δ-tocopherols are nontoxic and dietary tocopherols, especially δ-tocopherol, can limit several BEC and LEC endothelial behaviors associated with angiogenesis. Tocopherols may therefore represent important nutrient-signals that limit cell behaviors related to inflammation/angiogenesis, which when deficient, may predispose individuals to risks associated with elevated angiogenesis such as inflammation and cancer; further differences seen from the tocopherols may be due to their blood or lymphatic cell origin. © 2010.


Trademark
YASOO Health Inc. | Date: 2011-04-05

Pharmaceuticals in the nature of dietary iron supplements for medical use.


Trademark
YASOO Health Inc. | Date: 2012-11-06

Pharmaceuticals in the nature of dietary supplements for medical use.


Trademark
YASOO Health Inc. | Date: 2014-09-15

Nutritional supplements.


Trademark
YASOO Health Inc. | Date: 2012-03-30

Dietary supplements for medical use.


PubMed | Yasoo Health Ltd.
Type: Comparative Study | Journal: Nutrition and cancer | Year: 2010

Current observations in the literature suggest that vitamin E may be a suitable candidate for cancer chemotherapy. To investigate this further, we examined the ability of the vitamin E natural homologs [alpha-, beta-, gamma-, delta-tocopherols (alpha-TOC, beta-TOC, gamma-TOC, delta-TOC) and alpha-, beta-, gamma-, delta-tocotrienols (alpha-TT, beta-TT, gamma-TT, delta-TT)] and their corresponding succinate synthetic derivatives [alpha-, beta-, gamma-, delta-tocopheryl succinates and alpha-, beta-, gamma-, delta-tocotrienyl succinates (alpha-TS, beta-TS, gamma-TS, delta-TS)] to induce cell death in AR- (DU145 and PC3) and AR+ (LNCaP) prostate cancer cell lines. The most effective of all the natural homologs of vitamin E was determined to be delta-TT, whereas delta-TS was the most potent of all the natural and synthetic compounds of vitamin E examined. Both gamma-TT and delta-TT induced caspase activity selectively in AR+ LNCaP cells, suggesting a possible role for AR for the activation of caspase-dependent programmed cell death (CD-PCD). More important, however, gamma-TT, delta-TT, gamma-TS, and delta-TS activated dominant caspase-independent programmed cell death (CI-PCD) in all prostate cancer cell lines examined. Thus, vitamin E homologs and synthetic derivatives may find applications in the treatment of prostate tumors that are resistant to caspase-activating therapeutic agents.


PubMed | Yasoo Health Ltd.
Type: Journal Article | Journal: Nutrition and cancer | Year: 2012

Vitamin E comprises 8 functionally unique isoforms and may be a suitable candidate for the adjuvant treatment of prostate cancer. In this study, we examined the ability of 2 vitamin E isoforms [-tocotrienol (-TT) and -tocotrienol (-TT)] and 4 synthetic derivatives [- and -tocotrienol succinate (-TS, -TS), -tocopheryl polyethylene glycol succinate (TPGS), and -tocopheryl polyethylene glycol ether (TPGS-e)] of vitamin E to induce cell death in AR- (DU145 and PC-3) and AR+ (LNCaP) prostate cancer cell lines. Our results show that -TT and TPGS-e are the most effective isoform and synthetic derivative, respectively, of all compounds examined. Overall, the results of our study suggest that isoforms and synthetic derivatives of vitamin E have the potency to trigger both caspase-dependent and -independent DNA damage and dominant caspase-independent programmed cell death. The capacity of vitamin E to trigger caspase-independent programmed cell death suggests that it may be useful in the chemotherapy of prostate cancer since it may prevent the tumor resistance commonly associated with the use of classical chemotherapeutic agents that trigger caspase-dependent programmed cell death.

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