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

Journal Article · Sun May 15 04:00:00 EDT 2005 · Experimental Cell Research

DOI:https://doi.org/10.1016/j.yexcr.2005.01.019· OSTI ID:20717594

Pillich, Rudolf Tito ^[1]; Scarsella, Gianfranco ^[1]; Risuleo, Gianfranco ^[2]

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1. Dipartimento di Biologia Cellulare e dello Sviluppo (Italy)
2. Dipartimento di Genetica e Biologia Molecolare, Universita di Roma 'La Sapienza', P.le A. Moro, 5-00185 Rome (Italy)

It is shown in literature that stress, such as deprivation of trophic factors and hypoxia, induces apoptosis in cultured cells and in tissues. In light of these results, we explored the possibility of protecting cells from programmed death by improving the metabolism of the mitochondrion. To this end, acetyl-L-carnitine was administered at various concentrations under conditions of serum deprivation. The choice of this drug was based on the accepted notion that acetyl-L-carnitine is able to stabilize mitochondrial membranes and to increase the supply of energy to the organelle. The results presented here indicate that the drug protects cells from apoptotic death: this is demonstrated by a lower positivity to the TUNEL reaction and by a strong reduction of the apoptotic DNA ladder in serum-deprived cells. The involvement of the mitochondrial apoptotic pathway was assessed by cytochrome C release and immunoreactivity to caspase 3. Moreover, acetyl-L-carnitine stimulates cell proliferation.

• OSTI ID: 20717594
• Journal Information: Experimental Cell Research, Journal Name: Experimental Cell Research Journal Issue: 1 Vol. 306; ISSN 0014-4827; ISSN ECREAL
• Country of Publication: United States
• Language: English

Related Subjects

60 APPLIED LIFE SCIENCES
ANOXIA
ANTIGENS
APOPTOSIS
BIOLOGICAL STRESS
CARNITINE
CELL CONSTITUENTS
CELL PROLIFERATION
DNA
DRUGS
FIBROBLASTS
LABELLING
METABOLISM
MICE