Figure 2
From: Oxidative stress induces mitochondrial dysfunction in a subset of autistic lymphoblastoid cell lines
Lymphoblastoid cell lines (LCLs) derived from children with autistic disorder (AD) demonstrate differences in mitochondrial function as compared with control LCLs at baseline and after exposure to the redox cycling agent 2,3-dimethoxy-1,4-napthoquinone (DMNQ) at four concentrations (5, 10, 12.5 and 15 μM) one hour before the assay. (a) Basal respiration increases as DMNQ concentration increases in the AD LCLs and becomes significantly higher in the AD LCLs at 10 and 12.5 μM DMNQ; (b) adenosine-5’-triphosphate-linked respiration increases as DMNQ concentration increases in the AD LCLs and becomes significantly higher in the AD LCLs at 10 μM DMNQ; (c) proton-leak respiration increases as DMNQ concentration increases in the AD LCLs and becomes significantly higher in the AD LCLs at 10 and 12.5 μM DMNQ; (d) maximum respiratory capacity decreased as DMNQ increased for both AD and control LCLs but overall AD LCLs demonstrated a higher maximum respiratory capacity; (e) reserve capacity decreases as DMNQ increases for both AD and control LCLs but the decline in reserve capacity is much sharper for the AD LCLs as compared with the control LCLs due to the fact that reserve capacity is significantly higher in the AD LCLs at low DMNQ concentrations but becomes significantly lower in the AD LCL at higher DMNQ concentrations.
