Restoration of cellular energetic balance with L-carnitine in the neuro-bioenergetic approach for cancer prevention and treatment

被引:7
作者
Hoang, Ba X.
Shaw, D. Graeme
Pham, Phuong
Levine, Stephen
机构
[1] Allergy Res Grp, San Jose, CA 95117 USA
[2] Adv Integrat Med, Los Altos, CA 94022 USA
[3] Univ So Calif, Dept Mol Biol, Los Angeles, CA 90089 USA
[4] Allergy Res Grp, Alameda, CA 94502 USA
关键词
D O I
10.1016/j.mehy.2006.11.049
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Mitochondrial research has contributed to two paradigm shifts in oncology - Warburg's glycolytic metabolism and the relationship between mitochondrial function and mutagenesis. Mitochondrial dysfunction is a common phenotype in aging and cancer. Decline in mitochondrial function is due to the accumulation of mutations in mitochondrial DNA. We have hypothesized a neuro-bioenergetic concept in cancer prevention and treatment to constructively restore three physiological imbalances of cancer patients: membrane hyper-excitabitity, energy depletion and the build up of extra-cellular adenosine molecules. We have proposed the use of membrane-calming substances to reduce energy consumption and to restore the normal cellular energy metabolism. Based on our theory, L-carnitine's dual effect of enhanced energy production and excitatory neurotransmitter modulation should make it an ideal nutrient for cancer prevention and treatment. L-carnitine, its derivatives and other mitochondrial protectors/ enhancers improve metabolic function, energy and detoxification. In combination with other membrane calming agents, L-carnitine could help reverse the membrane hyper-excitability to overcome a neuro-bioenergetic imbalance and can be used as a relevant and effective approach for cancer
引用
收藏
页码:262 / 272
页数:11
相关论文
共 93 条
[1]   Acetyl-L-carnitine-induced up-regulation of heat shock proteins protects cortical neurons against amyloid-beta peptide 1-42-mediated oxidative stress and neurotoxicity: Implications for Alzheimer's disease [J].
Abdul, Hafiz Mohmmad ;
Calabrese, Vittorio ;
Calvani, Menotti ;
Butterfield, D. Allan .
JOURNAL OF NEUROSCIENCE RESEARCH, 2006, 84 (02) :398-408
[2]   L-carnitine in dialysis patients [J].
Ahmad, S .
SEMINARS IN DIALYSIS, 2001, 14 (03) :209-217
[3]   Mitochondrial stress-induced calcium signaling, phenotypic changes and invasive behavior in human lung carcinoma A549 cells [J].
Arnuthan, G ;
Biswas, G ;
Ananadatheerthavarada, HK ;
Vijayasarathy, C ;
Shephard, HM ;
Avadhani, NG .
ONCOGENE, 2002, 21 (51) :7839-7849
[4]  
Arrigoni-Martelli E, 2001, DRUG EXP CLIN RES, V27, P27
[5]   COENZYME Q(10) AND NICOTINAMIDE BLOCK STRIATAL LESIONS PRODUCED BY THE MITOCHONDRIAL TOXIN MALONATE [J].
BEAL, MF ;
HENSHAW, DR ;
JENKINS, BG ;
ROSEN, BR ;
SCHULZ, JB .
ANNALS OF NEUROLOGY, 1994, 36 (06) :882-888
[6]   Symptomatic and neurophysiological responses of paclitaxel- or cisplatin-induced neuropathy to oral acetyl-L-carnitine [J].
Bianchi, G ;
Vitali, G ;
Caraceni, A ;
Ravaglia, S ;
Capri, G ;
Cundari, S ;
Zanna, C ;
Gianni, L .
EUROPEAN JOURNAL OF CANCER, 2005, 41 (12) :1746-1750
[7]   Saving erythropoietin by administering L-carnitine? [J].
Bommer, J .
NEPHROLOGY DIALYSIS TRANSPLANTATION, 1999, 14 (12) :2819-2821
[8]   L-carnitine as an ergogenic aid for patients with chronic obstructive pulmonary disease submitted to whole-body and respiratory muscle training programs [J].
Borghi-Silva, A ;
Baldissera, V ;
Sampaio, LMM ;
Pires-DiLorenzo, VA ;
Jamami, M ;
Demonte, A ;
Marchini, JS ;
Costa, D .
BRAZILIAN JOURNAL OF MEDICAL AND BIOLOGICAL RESEARCH, 2006, 39 (04) :465-474
[9]   CARNITINE - METABOLISM AND FUNCTIONS [J].
BREMER, J .
PHYSIOLOGICAL REVIEWS, 1983, 63 (04) :1420-1480
[10]  
Brevetti G, 1997, MUSCLE NERVE, V20, P1115, DOI 10.1002/(SICI)1097-4598(199709)20:9<1115::AID-MUS4>3.0.CO