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Miscellaneous

Corrigendum

Page 193 | Published online: 07 Jul 2009
This article refers to:
Lipid peroxidation, mitochondrial dysfunction and neurochemical and behavioural deficits in different neurotoxic models: Protective role of S-allylcysteine

The authors would like to apologise for an error that occurred in the publication of Free Radical Research, October 2008; 42(10): 892–902.

Lipid peroxidation, mitochondrial dysfunction and neurochemical and behavioural deficits in different neurotoxic models: Protective role of S-allylcysteine

ESPERANZA GARCIA, DANIEL LIMON, VERONICA PEREZ-DE LA CRUZ, MAGDA GIORDANO, MAURICIO DIAZ-MUÑOZ, PERLA D. MALDONADO, MARIA NIEVES HERRERA-MUNDO, JOSE PEDRAZA-CHAVERRI, & ABEL SANTAMARIA

The Figure 1 caption contained errors and should have read:

Figure 1. Effect of S-allylcysteine (SAC) on different markers of 1-methyl-4 phenyl-1,2,3,6-tetrahydropiridinium (MPTP)-induced striatal toxicity. SAC (30, 60 or 120 mg kg − 1, i.p.) was administered to mice for five consecutive days, 30 min before the administration of MPTP (30 mg kg − 1, i.p.). In (A) SAC prevented the MPTP-induced lipoperoxidation in mice synaptosomal fractions in a concentration-dependent manner; (B) SAC ameliorated the MPTP-induced disrupted mitochondrial reductive capacity in mice synaptosomal fractions in a concentration-dependent manner; (C) SAC attenuated the MPTP-induced dopamine depletion in mice striatal tissue in a concentration-dependent manner; (D) SAC reduced the MPTP-induced low motility pattern in mice. All markers were evaluated seven days after the last MPTP administration. For all graphics, mean values±SEM of 9–10 experiments per group are presented. *p<0.05 and **p<0.01, statistically different of Control;+p<0.05 and + +p<0.01, different of MPTP alone; one-way ANOVA followed by Tukey's test.

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