l-Carnitine and some of its analogs delay the onset of apoptotic cell death initiated in murine C2.8 hepatocytic cells after hepatocyte growth factor deprivation

Revoltella, Roberto P.; Canto, Beatrice Dal; Caracciolo, Lorenza; C, D'Urso

doi:10.1016/0167-4889(94)90265-8

Cited by 22 publications

(10 citation statements)

References 17 publications

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“…L-carnitine has been recently shown to act as an important antiapoptotic mediator (Ishii et al 2000;Moretti et al 2002). Inhibition of apoptosis by L-carnitine has been reported in primary cultured neuronal cells (Ishii et al 2000), nonneuronal cell lines like P 19 teratoma cells (Galli and Fratelli, 1993) and C2.8 hepatocyte (Revoltella et al 1994). L-carnitine enhances the activity of the DNA repairing enzyme poly(ADP-ribosyl) polymerase and other related repair mechanisms (Boerrigter et al 1993).…”

Section: Discussionmentioning

confidence: 97%

Antiapoptotic effect of l-carnitine on testicular irradiation in rats

2010

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We evaluated the effects of L-carnitine on apoptosis of germ cells in the rat testis following irradiation. Male Wistar rats were divided into three groups. Control group received sham irradiation plus physiological saline. Radiotherapy group received scrotal gamma-irradiation of 10 Gy as a single dose plus physiological saline. Radiotherapy + L-carnitine group received scrotal irradiation plus 200 mg/kg intraperitoneally L-carnitine. Twenty-four hours post-irradiation, the rats were sacrificed and testes were harvested. Testicular damage was examined by light and electron microscopy, and germ cell apoptosis was determined by terminal deoxynucleotidyltransferase-mediated deoxyuridine triphosphate in situ nick end-labeling (TUNEL) technique. Morphologically, examination of irradiated testis revealed presence of disorganization and desquamation of germinal cells and the reduction in sperm count in seminiferous tubule lumen. Under electron microscopy, the morphological signs of apoptosis were frequently detected in spermatogonia. Apoptotic spermatogonia showed the marginal condensation of chromatin onto the nuclear lamina, nucleus and cytoplasm shrinkage and still functioning cell organelles. TUNEL-positive cells were significantly more numerous in irradiated rats than in control rats. L-carnitine treatment significantly attenuated the radiation-induced morphological changes and germ cell apoptosis in the irradiated rat testis. In conclusion, these results suggested that L-carnitine supplementation during the radiotherapy may be beneficial for spermatogenesis following testicular irradiation by decreasing germ cell apoptosis.

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Section: Discussionmentioning

confidence: 97%

Antiapoptotic effect of l-carnitine on testicular irradiation in rats

2010

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“…Literature data show that growth factors may antagonize apoptosis; with respect to this, ALC was shown to stimulate the activity of different growth factors such as, for example, hepatocyte growth factor (HGF) and neuronal growth factor (NGF) [29,30]. In particular, the apoptosis protective action of fibroblast growth factors FGF-2 and bFGF has recently been shown [6,31].…”

Section: Discussionmentioning

confidence: 97%

Reduction of apoptosis through the mitochondrial pathway by the administration of acetyl-l-carnitine to mouse fibroblasts in culture

Pillich

Scarsella

Risuleo

2005

Experimental Cell Research

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“…The increase in fatty acid oxidation induced by AICAR has been shown to result from a stimulation in the activities of both CPT-1 (47) and malonylCoA decarboxylase (35), the enzyme which degrades malonylCoA, the allosteric inhibitor of carnitine palmitoyltransferase I. In several systems, CPT-1 can protect from palmitate-triggered cell death (10,48,49). The protection from palmitate-induced apoptosis afforded by CPT-1 is most likely to be the consequence of palmitoyl-CoA clearance from the cytoplasm, because the CPT enzyme complex effectively transfers long chain fatty acyl-CoA into the mitochondrial matrix, where they serve as fuel for ␤-oxidation.…”

Section: Discussionmentioning

confidence: 99%

Saturated Fatty Acid-induced Apoptosis in MDA-MB-231 Breast Cancer Cells

Hardy

El-Assaad

Przybytkowski

et al. 2003

Journal of Biological Chemistry

246

243

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Little is known about the biochemical basis of the action of free fatty acids (FFA) on breast cancer cell proliferation and apoptosis. Here we report that unsaturated FFAs stimulated the proliferation of human MDA-MB-231 breast cancer cells, whereas saturated FFAs inhibited it and caused apoptosis. Saturated FFA palmitate decreased the mitochondrial membrane potential and caused cytochrome c release. Palmitate-induced apoptosis was enhanced by the fat oxidation inhibitor etomoxir, whereas it was reduced by fatty-acyl CoA synthase inhibitor triacsin C. The non-metabolizable analog 2-bromopalmitate was not cytotoxic. This indicates that palmitate must be metabolized to exert its toxic effect but that its action does not involve fat oxidation. Pharmacological studies showed that the action of palmitate is not mediated via ceramides, reactive oxygen species, or changes in phosphatidylinositol 3-kinase activity. Palmitate caused early enhancement of cardiolipin turnover and decreased the levels of this mitochondrial phospholipid, which is necessary for cytochrome c retention. Cosupplementation of oleate, or increasing ␤-oxidation with the AMP-activated protein kinase activator, 5-aminoimidazole-4-carboxamide-1-␤-D-ribonucleoside, both restored cardiolipin levels and blocked palmitate-induced apoptosis. Oleate was preferentially metabolized to triglycerides, and oleate cosupplementation channeled palmitate esterification processes to triglycerides. Overexpression of Bcl-2 family members blocked palmitateinduced apoptosis. The results provide evidence that a decrease in cardiolipin levels and altered mitochondrial function are involved in palmitate-induced breast cancer cell death. They also suggest that the antiapoptotic action of oleate on palmitate-induced cell death involves both restoration of cardiolipin levels and redirection of palmitate esterification processes to triglycerides.

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l-Carnitine and some of its analogs delay the onset of apoptotic cell death initiated in murine C2.8 hepatocytic cells after hepatocyte growth factor deprivation

Cited by 22 publications

References 17 publications

Antiapoptotic effect of l-carnitine on testicular irradiation in rats

Antiapoptotic effect of l-carnitine on testicular irradiation in rats

Reduction of apoptosis through the mitochondrial pathway by the administration of acetyl-l-carnitine to mouse fibroblasts in culture

Saturated Fatty Acid-induced Apoptosis in MDA-MB-231 Breast Cancer Cells

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