Some more:
College of Pharmacy and Pharmaceutical Sciences, Florida A & M University, Tallahassee, FL 32307, USA.
Acetyl-L-carnitine (ALCAR) plays an integral role in the transport of long chain fatty acids across the inner mitochondrial membrane for oxidative phosphorylation. In non-human primates, administration of ALCAR was reported to prevent 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurological injury to the substantia nigra. The present study investigates the effects of ALCAR against the toxicity of 1-methyl-4-phenylpyridinium (MPP(+)), the neurotoxic metabolite of MPTP, in murine brain neuroblastoma cells. MPP(+), a potent mitochondrial toxin, induced a dose-dependent reduction in mitochondrial oxygen consumption and cell viability, corresponding to an accelerated rate of cellular glucose utilization. Treatment with ALCAR, but not L-carnitine, prevented MPP(+) toxicity and partially restored intracellular ATP concentrations, but did not reverse the MPP(+)-induced loss of mitochondrial oxygen consumption. These data indicate that protective effects are independent of oxidative phosphorylation. ALCAR had a substantial glucose sparing effect in both controls and MPP(+)-treated groups, demonstrating a potential role in enhancing glucose utilization through glycolysis. Antagonizing the entry of fatty acids into the mitochondria, with either insulin or malonyl CoA, did not interfere with ALCAR protection against MPP(+). On the contrary, insulin potentiated the protective effects of ALCAR. In conclusion, these data indicate that ALCAR protects against MPP(+) toxicity, independent of mitochondrial oxidative capacity or beta-oxidation of fatty acids. In contrast, the protective effects of ALCAR appear to involve potentiation of energy derived from glucose through anaerobic glycolysis.
Blond-McIndoe Centre, Royal Free and University College Medical School, University Department of Surgery, Royal Free Campus, Rowland Hill Street, London NW3 2PF, UK.
Peripheral nerve trauma remains a major cause of morbidity, largely due to the death of approximately 40% of innervating sensory neurons, and to slow regeneration after repair. Acetyl-L-carnitine (ALCAR) is a physiological peptide that virtually eliminates sensory neuronal death, and may improve regeneration after primary nerve repair. This study determines the effect of ALCAR upon regeneration after secondary nerve repair, thereby isolating its effect upon neuronal regenerative capacity. Two months after unilateral sciatic nerve division 1 cm nerve graft repairs were performed (n=5), and treatment with 50 mg/kg/day ALCAR was commenced for 6 weeks until harvest. Regeneration area and distance were determined by quantitative immunohistochemistry. ALCAR treatment significant increased immunostaining for both nerve fibres (total area 264% increase, P<0.001; percentage area 229% increase, P<0.001), and Schwann cells (total area 111% increase, P<0.05; percentage area 86% increase, P<0.05), when compared to no treatment. Regeneration into the distal stump was greatly enhanced (total area 2,242% increase, P=0.008; percentage area 3,034% increase, P=0.008). ALCAR significantly enhances the regenerative capacity of neurons that survive peripheral nerve trauma, in addition to its known neuroprotective effects.
Department of Applied Chemistry and Biotechnology, Faculty of Engineering, Yamanashi University, Yamanashi 400-8511, Japan.
In the present study, we examined the effects of acetyl-L-carnitine (ALC) on the brain lipid hydroperoxide level and on passive avoidance performance in senescence-acceleration-prone 8 mice (SAMP8). Mice were treated intraperitoneally with either saline or ALC (100 or 400 mg/kg) three times a week up to 4 months of age (starting at 3 weeks of age). In 4-month-old SAMP8, the deficit in learning and memory seen in saline-treated controls was significantly ameliorated in 400 mg/kg ALC-treated SAMP8, and the brain lipid hydroperoxide level was significantly lower in the 400 mg/kg ALC-treated group than in the saline-treated controls. Administration of 100 mg/kg ALC to SAMP8 did not have significant effect on learning and memory performance or on the brain lipid hydroperoxide level (by comparison with the saline-treated controls). These results suggest that ALC has antioxidant activity towards oxidative stress, and that the improvement in cognitive ability seen with ALC may occur through an amelioration of cellular dysfunction via an inhibition of the increase in lipid hydroperoxidation observed in the brain tissue of untreated SAMP8
Center for Neurobiology and Neurodegeneration Research, University of Massachusetts Lowell, Lowell, Massachusetts 01854, USA.
[email protected]
Acetyl-L-carnitine (ALCAR), normally produced in mitochondria, is a precursor of acetyl-CoA in the tricarboxylic (TCA) cycle. Since mitochondrial compromise and ATP depletion have been considered to play a role in neuronal degeneration in Alzheimer's disease (AD), we examined whether ALCAR attenuated oxidative stress and/or ATP depletion after exposure of cells to beta-amyloid (Abeta), a neurotoxic peptide that accumulates in AD brain. Differentiated SH-SY-5Y human neuroblastoma cells were exposed for 2-24 h to 20 microM Abeta in the presence and absence of 50 microM ALCAR. ALCAR attenuated oxidative stress and cell death induced by Abeta neurotoxicity. Abeta depleted ATP levels, suggesting Abeta may induce neurotoxicity in part by compromising neuronal energy. ALCAR prevented ATP depletion; therefore, ALCAR may mediate its protective effect by buffering oxidative stress and maintaining ATP levels.
I'm taking in 3-4g's ALCar now...it's a truly great compound! If you're an athlete this is cardinal to combat innervation and harmful metabolites produced under stress (physical and mental, too)
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