Journal of nephrology · 2011
L-Carnitine attenuates ifosfamide-induced carnitine deficiency and decreased intramitochondrial CoA-SH in rat kidney tissues.
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Sayed-Ahmed Mohamed M
Аннотация
BACKGROUND: The effects of L-carnitine on ifosfamide (IFO)-induced Fanconi syndrome have not been studied to date. This study aimed to investigate, on a mechanism basis, whether L-carnitine could prevent the development of IFO-induced Fanconi syndrome in rats.
METHODS: Adult male Wistar albino rats were assigned to 1 of 4 treatment groups: group 1 (control) rats were given daily intraperitoneal (i.p.) injections of normal saline for 10 consecutive days; group 2 (L-carnitine) rats were given L-carnitine (200 mg/kg per day, i.p.) for 10 consecutive days. Rats of group 3 (IFO) received normal saline for 5 days, followed by IFO (50 mg/kg per day, i.p.) for 5 consecutive days. Rats of group 4 (IFO plus L-carnitine) received L-carnitine for 5 days before and 5 days concomitant with IFO.
RESULTS: Administration of IFO for 5 consecutive days significantly increased serum creatinine, blood urea nitrogen (BUN), urinary carnitine excretion, intramitochondrial acetyl-CoA and thiobarbituric acid reactive substances (TBARS), and significantly decreased total carnitine, intramitochondrial CoA-SH, ATP and ATP/ADP ratio, and reduced glutathione (GSH) in kidney tissues. Administration of L-carnitine to IFO-treated rats resulted in a complete reversal of the increase in serum creatinine, BUN, urinary carnitine excretion and intramitochondrial acetyl-CoA, and of the decrease in total carnitine, intramitochondrial CoA-SH, ATP and GSH, induced by IFO, to the control values.
CONCLUSIONS: L-Carnitine prevents the development of IFO-induced Fanconi syndrome by increasing intracellular carnitine content and intramitochondrial CoA-SH, with the consequent improvement in mitochondrial oxidative phosphorylation and energy production, as well as its ability to decrease oxidative stress.
METHODS: Adult male Wistar albino rats were assigned to 1 of 4 treatment groups: group 1 (control) rats were given daily intraperitoneal (i.p.) injections of normal saline for 10 consecutive days; group 2 (L-carnitine) rats were given L-carnitine (200 mg/kg per day, i.p.) for 10 consecutive days. Rats of group 3 (IFO) received normal saline for 5 days, followed by IFO (50 mg/kg per day, i.p.) for 5 consecutive days. Rats of group 4 (IFO plus L-carnitine) received L-carnitine for 5 days before and 5 days concomitant with IFO.
RESULTS: Administration of IFO for 5 consecutive days significantly increased serum creatinine, blood urea nitrogen (BUN), urinary carnitine excretion, intramitochondrial acetyl-CoA and thiobarbituric acid reactive substances (TBARS), and significantly decreased total carnitine, intramitochondrial CoA-SH, ATP and ATP/ADP ratio, and reduced glutathione (GSH) in kidney tissues. Administration of L-carnitine to IFO-treated rats resulted in a complete reversal of the increase in serum creatinine, BUN, urinary carnitine excretion and intramitochondrial acetyl-CoA, and of the decrease in total carnitine, intramitochondrial CoA-SH, ATP and GSH, induced by IFO, to the control values.
CONCLUSIONS: L-Carnitine prevents the development of IFO-induced Fanconi syndrome by increasing intracellular carnitine content and intramitochondrial CoA-SH, with the consequent improvement in mitochondrial oxidative phosphorylation and energy production, as well as its ability to decrease oxidative stress.