Table 4.

Effect of ifosfamide (IFO), propionyl-l-carnitine (pLC), D-carnitine-mildronate (DC-MD) and their combination on the levels of thiobarbituric acid reactive substances (TBARS) and reduced glutathione (GSH) in rat cardiac tissues.

Treatment groups	TBARS (nmol/g wet tissue)	GSH (µmol/g wet tissue)
Control	249.60 ± 14.9	0.70 ± 0.02
DC-MD	118.01 ± 14.7*	1.02 ± 0.09
PLC	113.21 ± 9.7*	1.23 ± 0.14*
IFO	449.14 ± 33.9*	0.280 ± 0.03*
IFO plus DC-MD	249.10 ± 33.8*#$	0.90 ± 0.08$
IFO plus PLC	243.60 ± 24.8#	0.89 ± 0.09#

Rats were randomly divided into 6 different groups of 10 animals each: Control, D-carnitine-mildronate (DC-MD, carnitine-depleted group), PLC (carnitine supplemented group), IFO, DC-MD plus IFO and PLC plus IFO. Carnitine depletion was induced in rats by daily intraperitoneal injection of DC (250 mg/kg/day) combined with MD (200 mg/kg/day) for 10 successive days. Carnitine supplementation was induced in rats by daily intraperitoneal injection of PLC (250 mg/kg/day) for 10 successive days. Fanconi Syndrome was induced in rats by administration of IFO (50 mg/kg/day, I.P.) for 5 successive days. IFO-carnitine depleted rats were given the same doses of DC-MD for 5 days before and 5 days concomitant with IFO. IFO-carnitine supplemented rats were given the same doses of PLC for 5 days before and 5 days concomitant with IFO. At the end of the treatment protocol, TBARS and GSH, oxidative stress biomarkers, were measured in rat cardiac tissues. Data are presented as mean ± S.E.M. (n = 10). ^*, ^# and ^$ indicate significant change from control, IFO and DC-MD respectively, at p < 0.05 using ANOVA followed by Tukey-Kramer as a post ANOVA test. Data are presented as mean ± S.E.M. (n = 10). ^*, ^# and ^$ indicate significant change from control, IFO and DC-MD respectively, at p < 0.05 using ANOVA followed by Tukey-Kramer as a post ANOVA test.