Protective actions of l-carnitine and acetyl-l-carnitine on the neurotoxicity evoked by mitochondrial uncoupling or inhibitors

Virmani, Ashraf; Biselli, Roberto; Spadoni, A.; Rossi, Stefania; Corsico, N.; Calvani, Menotti; Fattorossi, Andrea; Simone, Claudio De; Arrigoni-Martelli, E

doi:10.1016/s1043-6618(05)80044-1

Cited by 101 publications

(81 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Acetyl L-carnitine appears to be involved in the restoration of mitochondrial function and/or improved use of energy from glycolysis in cultured neuroblastoma cells treated with the neurotoxicant, 1-methyl-4-phenyl tetrahydropyridine (Mazzio et al, 2003). It has also been reported that rotenone-induced mitochondrial function inhibition can cause cell death in vitro in cultured rat cortical neurons that were, in part, prevented by the co-incubation of the cells with 1 mM acetyl Lcarnitine (Virmani et al, 1995). Carnitine has also been shown to effectively inhibit mitochondrial injury induced by oxidative stress and mitochondria-dependent apoptosis in various types of cells (Furuno et al, 2001;Hagen et al, 2002b;Therrien et al, 1997).…”

Section: Discussionmentioning

confidence: 99%

Acetyl l-carnitine protects motor neurons and Rohon-Beard sensory neurons against ketamine-induced neurotoxicity in zebrafish embryos

Cuevas

Trickler

Guo

et al. 2013

Neurotoxicology and Teratology

View full text Add to dashboard Cite

Ketamine, a non-competitive antagonist of N-methyl-D-aspartate (NMDA) type glutamate receptors is commonly used as a pediatric anesthetic. Multiple studies have shown ketamine to be neurotoxic, particularly when administered during the brain growth spurt. Previously, we have shown that ketamine is detrimental to motor neuron development in the zebrafish embryos. Here, using both wild type (WT) and transgenic (hb9:GFP) zebrafish embryos, we demonstrate that ketamine is neurotoxic to both motor and sensory neurons. Drug absorption studies showed that in the WT embryos, ketamine accumulation was approximately 0.4% of the original dose added to the exposure medium. The transgenic embryos express green fluorescent protein (GFP) localized in the motor neurons making them ideal for evaluating motor neuron development and toxicities in vivo. The hb9:GFP zebrafish embryos (28 h post fertilization) treated with 2 mM ketamine for 20 h demonstrated significant reductions in spinal motor neuron numbers, while co-treatment with acetyl L-carnitine proved to be neuroprotective. In whole mount immunohistochemical studies using WT embryos, a similar effect was observed for the primary sensory neurons. In the ketamine-treated WT embryos, the number of primary sensory Rohon-Beard (RB) neurons was significantly reduced compared to that in controls. However, acetyl L-carnitine co-treatment prevented ketamine-induced adverse effects on the RB neurons. These results suggest that acetyl L-carnitine protects both motor and sensory neurons from ketamine-induced neurotoxicity.

show abstract

Section: Discussionmentioning

confidence: 99%

Acetyl l-carnitine protects motor neurons and Rohon-Beard sensory neurons against ketamine-induced neurotoxicity in zebrafish embryos

Cuevas

Trickler

Guo

et al. 2013

Neurotoxicology and Teratology

View full text Add to dashboard Cite

show abstract

“…ALCAR participates in maintenance and repair processes in neurons, is able to attenuate the rate of neuronal mortality (Manfridi et al 1992) and to decrease the neurotoxicity evoked by mitochondrial uncoupling factors or inhibitors (Virmani et al 1995). ALCAR is also able to reduce the oxidative stress induced at the mitochondrial level by stimulant drug as 3,4-methylenedioximethamphetamine (Alves et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Antidepressant-like effect of artemin in mice: a mechanism for acetyl-l-carnitine activity on depression

et al. 2011

View full text Add to dashboard Cite

show abstract

“…ALCAR treatment ameliorates mitochondrial dysfunction caused by a variety of neurotoxic insults (Virmani et al, 1995(Virmani et al, , 2005Bertamini et al, 2002;Hart et al, 2004a;Sayed-Ahmed et al, 2004;Calabrese et al, 2005;Binienda et al, 2006;Mansour, 2006;Wang et al, 2007). Paclitaxel also causes degeneration of the sensory neurons' intraepidermal terminal arbors, without degeneration of the parent axons in the peripheral nerve, and it activates cutaneous Langerhans cells .…”

Section: Introductionmentioning

confidence: 99%

Prevention of paclitaxel-evoked painful peripheral neuropathy by acetyl-l-carnitine: Effects on axonal mitochondria, sensory nerve fiber terminal arbors, and cutaneous Langerhans cells

Jin

Flatters

Xiao

et al. 2008

Experimental Neurology

143

132

View full text Add to dashboard Cite

Prophylactic treatment with acetyl-L-carnitine (ALCAR) prevents the neuropathic pain syndrome that is evoked by the chemotherapeutic agent, paclitaxel. The paclitaxel-evoked pain syndrome is associated with degeneration of the intraepidermal terminal arbors of primary afferent neurons, with the activation of cutaneous Langerhans cells, and with an increased incidence of swollen and vacuolated axonal mitochondria in A-fibers and C-fibers. Previous work suggests that ALCAR is neuroprotective in other nerve injury models and that it improves mitochondrial dysfunction. Thus, we examined whether the prophylactic efficacy of ALCAR was associated with the prevention of intraepidermal terminal arbor degeneration, the inhibition of Langerhans cell activation, or the inhibition of swelling and vacuolation of axonal mitochondria. In animals with a confirmed ALCAR effect, we found no evidence of a neuroprotective effect on the paclitaxel-evoked degeneration of sensory terminal arbors or an inhibition of the paclitaxel-evoked activation of Langerhans cells. However, ALCAR treatment completely prevented the paclitaxel-evoked increase in the incidence of swollen and vacuolated C-fiber mitochondria, while having no effect on the paclitaxel-evoked changes in A-fiber mitochondria. Our results suggest that the efficacy of prophylactic ALCAR treatment against the paclitaxel-evoked pain may be related to a protective effect on C-fiber mitochondria.

show abstract

Protective actions of l-carnitine and acetyl-l-carnitine on the neurotoxicity evoked by mitochondrial uncoupling or inhibitors

Cited by 101 publications

References 24 publications

Acetyl l-carnitine protects motor neurons and Rohon-Beard sensory neurons against ketamine-induced neurotoxicity in zebrafish embryos

Acetyl l-carnitine protects motor neurons and Rohon-Beard sensory neurons against ketamine-induced neurotoxicity in zebrafish embryos

Antidepressant-like effect of artemin in mice: a mechanism for acetyl-l-carnitine activity on depression

Prevention of paclitaxel-evoked painful peripheral neuropathy by acetyl-l-carnitine: Effects on axonal mitochondria, sensory nerve fiber terminal arbors, and cutaneous Langerhans cells

Contact Info

Product

Resources

About