江苏龙网

  1. 首页 > 生活 > >

小小健康食堂管家|NADH过量不但不延寿，还折寿！NADH过量的三点危害，你知道吗？( 四 )


[23] Kuhn W, Muller T, Winkel R, Danielczik S, Gerstner A, Hacker R, Mattern C, and Przuntek H. Parenteral application of NADH in Parkinson’s disease: clinical improvement partially due to stimulation of endogenous levodopa biosynthesis. J Neural Transm 103: 1187–1193, 1996.
[24] Birkmayer, J. G., C. Vrecko, D. Volc & W. Birkmayer: Nicotinamide adenine dinucleotide (NADH)——a new therapeutic approach to Parkinson's disease. Comparison of oral and parenteral application. Acta Neurol Scand Suppl, 146, 32-5(1993).
[25] NASA: Stabilized NADH as a Countermeasure for Jet Lag. Report/Patent Number JSC-CN-6528.
[26] Forsyth, L. M., Preuss, H. G., MacDowell, A. L., Chiazze, L., Birkmayer, G. D., & Bellanti, J. A. (1999). Therapeutic effects of oral NADH on the symptoms of patients with chronic fatigue syndrome. Annals of Allergy, Asthma & Immunology, 82(2), 185–191.
[27] Alegre, J., Rosés, J. M., Javierre, C., Ruiz-Baqués, A., Segundo, M. J., & Fernández de Sevilla, T. (2010). Nicotinamida adenina dinucleótido (NADH) en pacientes con síndrome de fatiga crónica. Revista Clínica Espa?ola, 210(6), 284–288.
[28] Vis, J. C., E. Schipper, R. T. de Boer-van Huizen, M. M. Verbeek, R. M. de Waal, P. Wesseling, H. J. ten Donkelaar & B. Kremer: Expression pattern of apoptosis-related markers in Huntington's disease. Acta Neuropathol (Berl), 109, 321-8(2005).
[29] Virag, L. & C. Szabo: The therapeutic potential of poly (ADP-ribose) polymerase inhibitors. Pharmacol Rev, 54, 375-429(2002).
[30] Satchell, M. A., X. Zhang, P. M. Kochanek, C. E. Dixon, L. W. Jenkins, J. Melick, C. Szabo & R. S. Clark: A dual role for poly-ADP-ribosylation in spatial memory acquisition after traumatic brain injury in mice involving NAD+ depletion and ribosylation of 14-3-3gamma. J Neurochem, 85, 697-708(2003).
[31] LaPlaca, M. C., J. Zhang, R. Raghupathi, J. H. Li, F. Smith, F. M. Bareyre, S. H. Snyder, D. I. Graham & T. K. McIntosh: Pharmacologic inhibition of poly (ADP-ribose) polymerase is neuroprotective following traumatic brain injury in rats. J Neurotrauma, 18, 369-76(2001).
[32] Kofler, J., T. Otsuka, Z. Zhang, R. Noppens, M. R. Grafe, D. W. Koh, V. L. Dawson, J. M. de Murcia, P. D. Hurn & R. J. Traystman: Differential effect of PARP-2 deletion on brain injury after focal and global cerebral ischemia. J Cereb Blood Flow Metab, 26, 135-41(2006).
[33] Gilgun-Sherki, Y., E. Melamed & D. Offen: The role of oxidative stress in the pathogenesis of multiple sclerosis: the need for effective antioxidant therapy. J Neurol, 251, 261-8(2004).
[34] Kauppinen, T. M., S. W. Suh, C. P. Genain & R. A. Swanson: Poly (ADP-ribose) polymerase-1 activation in a primate model of multiple sclerosis. J Neurosci Res, 81, 190-8(2005).
[35] Tentori, L., I. Portarena, F. Torino, M. Scerrati, P. Navarra & G. Graziani: Poly (ADP-ribose) polymerase inhibitor increases growth inhibition and reduces G(2)/M cell accumulation induced by temozolomide in malignant glioma cells. Glia, 40, 44-54(2002).


推荐阅读


上一篇：内分泌疾病|关于健康方面的误区

下一篇：日本|《无人知晓》：在日本，每年有3万人因“孤独”而死