[Relationships between concentrations of free fatty acid in serum and oxidative-damage levels in placental mitochondria and preeclampsia].

OBJECTIVE: To investigate the relationships between concentrations of free fatty acid (FFA) in maternal serum and oxidative damage levels in placental mitochondria and preeclampsia (PE). METHODS: A total of 60 women with PE and 60 normal pregnant women as control participated in this study. All were admitted to Fujian Maternity and Child Health Hospital for delivery from August 2010 to May 2011. Patients with PE were divided into early-onset group (n = 30, presented at < 34 weeks of gestation) and late-onset group (n = 30, presented at ≥ 34 weeks of gestation), with 30 normal pregnant women as early control group (< 34 weeks of gestation) and 30 as late control group (≥ 34 weeks of gestation). Improved copper agent colorimetry was used to detect FFA in maternal serum. Ultraviolet colorimetry was used to detect glutathione peroxidase (GPX) and catalase (CAT) activity in maternal placenta and malondialdehyde (MDA) and permeability transition (PT) pore in placental mitochondria. Total superoxide dismutase (SOD) assay kit-WST was used to detect SOD activity in placenta. Real-time fluorescent quantitative PCR was used to detect mitochondrial DNA (mtDNA) expression in placenta. RESULTS: (1) Maternal serum FFA was (1.6 ± 0.5) mmol/L in early-onset PE group and (1.5 ± 0.4) mmol/L in late-onset PE group, significantly elevated as compared to (1.0 ± 0.5) mmol/L in early control group and (0.9 ± 0.5) mmol/L in late control group (P < 0.05). However, no significant difference was found between early-onset and late-onset PE groups (P > 0.05). (2) The mean placental GPX, CAT and SOD activity were significantly decreased in the early-onset PE group [(47 ± 6), (19 ± 5), (62 ± 13) U/mg] and late-onset PE group [(67 ± 6), (20 ± 4), (96 ± 17) U/mg] as compared to late control group [(80 ± 3), (55 ± 3), (123 ± 19) U/mg], respectively (P < 0.05). (3) The mean placental mitochondria MDA was significantly elevated in the early-onset PE group [(115 ± 22) nmol/mg] and late-onset PE group [(90 ± 17) nmol/mg] as compared to late control group [(52 ± 11) nmol/mg, P < 0.05]. The mean absorption value that present the permeability of placental mitochondria PT pore was significantly elevated in the early-onset PE group (0.086 ± 0.013) and late-onset PE group (0.069 ± 0.014) as compared to late control group (0.052 ± 0.012, P < 0.05). The mean placental mtDNA expression was significantly elevated in the early-onset PE group (3.0 ± 0.7) and late-onset PE group (2.8 ± 0.7) as compared to late control group (2.6 ± 0.6, P < 0.05). (4) The mean placental mitochondria MDA concentration correlated positively with the concentrations of FFA in maternal serum in the early-onset PE group (r = 0.703, P < 0.05) and late-onset PE group (r = 0.457, P < 0.05), and negatively with placental antioxidant enzyme in the early-onset PE group (r = -0.652, -0.787, -0.952; P < 0.05) and late-onset PE group (r = -0.378, -0.689, -0.854; P < 0.05). CONCLUSIONS: Increased FFA in maternal serum and high levels of oxidative damage in placental mitochondria may be involved in the pathogenesis of preeclampsia. Increased FFA in serum and decreased activity of antioxidant enzyme in placenta may contribute to oxidative damage levels in placental mitochondria in women with PE.