Protection from Oxygen Radical Damage in Human Diploid Fibroblasts by Acetyl-<i>L</i>-Carnitine

Abstract

Oxygen radical production is suspected of being a major cause of aging. We have studied the effect of acetyl-L-carnitine (ALC) on oxygen metabolites toxicity in fibroblast cell lines derived from skin biopsies taken from apparently normal subjects. Fibroblast damage was produced by the generation of oxygen metabolites during the enzymatic oxidation of acetaldehyde with 50 mU of xanthine oxidase (XO). We measured lactate dehydrogenase (LDH) activity in the culture medium and cell viability in fibroblast cultures, both 4 days preincubated with 50 µg/ml ALC and not treated, after a 2-hour XO incubation in order to quantify the cell damage. We found a significant increase of LDH activity in cells without ALC exposed to free radical formation. No significant increase of the LDH activity was observed in the same cell lines, in the same experimental conditions after 4 days’ preincubation with 50 µg/ml ALC.

Neuroprotective effects of acetyl‐L‐carnitine on neuropathic pain and apoptosis: A role for the nicotinic receptor

“…Furthermore, ALCAR is an endogenous molecule with a pivotal role in improving the energetic state of the cell, and it may prevent the failure of mitochondrial oxidative metabolism (Budd and Nicholls, 1998). Moreover, its antioxidant role may be of benefit in preventing cell damage by the reactive oxygen species, whose generation is thought to be of great importance in the effector mechanism of cell death (Tesco et al, 1992).…”

Comparison of the effects of aminoguanidine and L-carnitine treatments on somatosensorial evoked potentials in alloxan-diabetic rats

“…Previously, effects of AG or LC on SEP latencies have not been reported. It has also been reported that ALC enhances the activity of antioxidant factors, such as reduced glutathione, and protects the cell against lipid peroxidation (Tesco et al 1992). The reason for this weak effect of LC on SEP latency may be the limited ability of LC to pass through blood-brain barrier (Brooks and McIntosh 1975).…”

“…ALC is an endogenous substance similar in structure to acetylcholine and is involved in uptake and oxidation of long-chain fatty acids in mitochondria (Sass and Wermess 1973). ALC enhances the activity of antioxidant factors such as reduced glutathione, and protects the cell against lipid peroxidation (free radical scavenging effect) (Tesco et al 1992). A beneficial effect of ALC or LC on nerve function has also been demonstrated in animal diabetes (Malone et al 1992;Morabito et al 1993;Merry et al 1994;Ido et al 1994).…”

Acetyl-L-carnitine for symptomatic diabetic neuropathy

“…ALC has been shown to acutely increase the plasma concentration of the endogenous opioid peptide beta-endorphin in healthy volunteers (analgesic effect) [6]; ALC increases the number of nerve growth factor receptors on the brain and prevents substance P loss in the sciatic nerve and spinal cord of diabetic animals (neurotropic effect) [7]; ALC influences mitochondrial protein synthesis and transport and non-esterified fatty acid oxidation, thereby increasing the oxidative metabolism of neurons (metabolic effect) [5]; lastly, ALC enhances the activity of antioxidant factors, such as reduced glutathione, and protects the cells against lipid peroxidation (flee radical scavenging effect) [8]. ALC has been shown to acutely increase the plasma concentration of the endogenous opioid peptide beta-endorphin in healthy volunteers (analgesic effect) [6]; ALC increases the number of nerve growth factor receptors on the brain and prevents substance P loss in the sciatic nerve and spinal cord of diabetic animals (neurotropic effect) [7]; ALC influences mitochondrial protein synthesis and transport and non-esterified fatty acid oxidation, thereby increasing the oxidative metabolism of neurons (metabolic effect) [5]; lastly, ALC enhances the activity of antioxidant factors, such as reduced glutathione, and protects the cells against lipid peroxidation (flee radical scavenging effect) [8].…”