The enhanced cytotoxicity of HQ by Cu(II) could be completely prevented by adding BCS, glutathione (GSH), or dithiothreitol but not by catalase. solutions and support the hypothesis that hydroquinone moieties can reduce Fe(III) in natural waters. In addition, oxidation of HQ by Cu(II) also generated chemiluminescence. Metal-ion oxidations in solution. Article  As a chain carrying radical, SQ˙− continues to transfer an electron to molecular oxygen to yield the superoxide radical, followed by the generation of H2O2. NaBH 4) may be used for the reverse reaction. Learn more about Institutional subscriptions. The enhanced cytotoxicity of HQ by Cu(II) could be completely prevented by adding BCS, glutathione (GSH), or dithiothreitol but not by catalase. The redox process hydroquinone - quinone can be seen as a sequence of proton and electron transfers. The catalytic activity and selectivity in the Cu (II)–resin system increases compared to reaction without catalyst and with native Cu (II) ions. Katal., 1991, vol. of the whole article in a thesis or dissertation. x��]]s�Fv}�_�G�ֆ���y�Mv���Z������$&�M���}���/��ူ���B\4�����V�g�[�d哬���TکZ�ʻZ��|�n���6Տ�}�����t��z�˿��A����������~�믶��m~L� ���jm�t�r1��K�������J\?�����u����I�_����Ocw��_*��q�!�_�(Q��T�ˇ�M�]���V��r5KR�c�+��jdC���z'W�ǔ2������b���UsE���7��߄ppe���3�_M}e\�xn �q�\�w��//^J�~�ĉ2�X�榁�I��L��Z�f_B�4��_�nkuC�A�}�w�P��r�1*Y+?�*�\���r���C�Zډr����%�;�گP(�W(T��J�I{J�P�a1�]�>WBw�-�ޛ�7O�JEd��د᪈� ^�C�c����Z/f#�>+�|�i2A����N\J��>�����s7|�k��A*u��S�%�q�K�+N���]y�w"|ao��7�싼w�Q��Kl��]�K �b�S�]:��8O?��ŏ�zq��/�zچ:o|�|��ƴ?���X�\��;#`!ň��$�ļ�Tm-XK�"�s+�8�uֶ��������j��j]�T�՛�僤�+�o7��ס{���my���m��b\ In the presence of myeloperoxidase, Cu(II)-mediated oxidation of HQ was increased. Please enable JavaScript 4, pp. © 2020 Springer Nature Switzerland AG. ChemInform Abstract: Oxidation of Hydroquinones and Hydroquinone Monomethyl Ethers to Quinones with tert‐Butyl Hydroperoxide and Catalytic Amounts of Ceric Ammonium Nitrate (CAN).. A New Gold‐Catalyzed Domino Cyclization and Oxidative Coupling Reaction. Addition of Cu(II) to primary bone marrow stromal cell cultures significantly enhanced HQ-induced cytotoxicity. If you are the author of this article you do not need to formally request permission and Afanas’ev, I.B., Oxidation and Antioxidants in Organic Chemistry and Biology, Boca Raton, Fla.: Taylor and Francis, 2005. D. Zhang, W. Shi, Q. Cheng, X. Li and A. Xu, School of Environmental Engineering, Wuhan Textile University, Wuhan 430200, China, School of Chemistry and Chemical Engineering, Wuhan Textile University, Wuhan 430200, China, Engineering Research Center for Clean Production of Dyeing and Printing, Ministry of Education, Wuhan Textile University, Wuhan, China, Instructions for using Copyright Clearance Center page. Please check your email for instructions on resetting your password. is available on our Permission Requests page. The Co(ii)–HCO3− system is much more efficient in the oxidation of H2Q than HCO3−, Co(ii)–OH− or othe 6, p. 1302. Pozdeeva, N.N., Yakushchenko, I.K., Aleksandrov, A.L, and Denisov, E.T., Kinet. Information about reproducing material from RSC articles with different licences When the peroxidation reaction was followed at the absorbance maxima of the corresponding benzoquinones (Q, DMQ, TMQ) a distinct lag phase was Paderborn, Universität, Fachbereich Chemie und Chemietechnik . AU - Trush, Michael A. PY - 1993/1 and Denisov, E.T., Kinet. Supplementation of stromal cells with 20 μM BCS in the absence of exogenously added Cu(II) significantly abated HQ-induced cellular GSH depletion and cytotoxicity, suggesting a possible involvement of endogenous copper in the activation of HQ. Number of times cited according to CrossRef: Strategies and Solutions to Advanced Organic Reaction Mechanisms. "�Q��й����;�n�X�(�4��x��9���h��o�BF��#yY��B���`J��K{�Z��d9T�ul��Ⱦ���Ź��#���B�$�E�/�B�����r���v� ����v� /]rY���̣��.b&S��%Ǘ��E��+}Z���_� u�q��p����wK�T�����p-ω�_,q��߹C�D�sQ聋��r�]Y����q�9�o���ƕ�xs=�To>� �|����m�hA�ߘ���n��:�kh���k,1�(6#� Similar to hydroquinone, the reaction of the DEHA with dissolved oxygen is Research output: Contribution to journal › Article › peer-review. The oxidation of HQ by Cu(II) could be blocked by the Cu(I)-specific chelator bathocuproinedisulfonic acid (ECS), particularly when the ratio of BCS to Cu(II) was 4:1. The oxidation of HQ by Cu(II) could be blocked by the Cu(I)-specific chelator bathocuproinedisulfonic acid (ECS), particularly when the ratio of BCS to Cu(II) was 4:1. E-mail address: kkcommat;chemie.uni‐paderborn.de. AU - Li, Yunbo B. Subrahmanyam VV(1), Kolachana P, Smith MT. CAS  The above results indicate that Cu(II) strongly induces the oxidation of HQ and as such may be a factor involved in the oxidative activation and toxicity of HQ in target cells. xahspinel@sina.com For reproduction of material from all other RSC journals and books: For reproduction of material from all other RSC journals. Mogilevich, M.M. In the soil, hydroquinone is expected to biodegrade under aerobic conditions. UR - http://www.scopus.com/inward/record.url?scp=0027259457&partnerID=8YFLogxK, UR - http://www.scopus.com/inward/citedby.url?scp=0027259457&partnerID=8YFLogxK, JO - Archives of Biochemistry and Biophysics, JF - Archives of Biochemistry and Biophysics, Powered by Pure, Scopus & Elsevier Fingerprint Engine™ © 2020 Elsevier B.V, "We use cookies to help provide and enhance our service and tailor content. Use the link below to share a full-text version of this article with your friends and colleagues. Supplementation of stromal cells with 20 μM BCS in the absence of exogenously added Cu(II) significantly abated HQ-induced cellular GSH depletion and cytotoxicity, suggesting a possible involvement of endogenous copper in the activation of HQ. The oxidation of acrylic acid inhibited by 4-methoxyphenol was studied under the same conditions for comparison. The activity of the catalysts was measured in the model reaction—oxidation of hydroquinone (H 2 Q) to p -benzoquinone (Q) by hydrogen peroxide (H 2 O 2 ). Transition Metal Chemistry 2009, 34 (3), 263-268. https://doi.org/10.1007/s11243-009-9188-x

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