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Susceptibility of placental mitochondria to oxidative stress
Rodrigo Papa Gobbi1, Gladis Magnarelli1,2, María Gabriela Rovedatti1
1Centro de Investigaciones en Toxicología Ambiental y Agrobiotecnología del Comahue (CITAAC), CONICET, Universidad Nacional del Comahue, Neuquén, Argentina.
Background:
Two different mitochondrial fractions (MFs) have been characterized in the human placenta: the "light" and "heavy" fractions (LMF and HMF). Although these organelles are the main source of reactive oxygen species, an imbalance between their production and the rate of detoxification represents a serious threat to mitochondrial homeostasis and, in the case of the placenta, also to the fetus. The aim of this study was to evaluate the antioxidant capacity and susceptibility to oxidative stress in both types of MFs.
Methods:
Human MFs were isolated from healthy donors (n = 11) and either incubated or not with H2 O2 . Catalase (CAT) activity, and reduced glutathione (GSH), lipid peroxidation (LP), and protein carbonylation (PC) levels were determined.
Results:
H2 O2 treatment increased LP and PC levels and decreased CAT activity. GSH levels were similar in control and treated MFs.
Conclusion:
H2 O2 caused oxidative damage in both LMF and HMF and the antioxidant system measured in these two MFs responded similarly. To the best of our knowledge, this is the first partial description of the antioxidant defense in placental HMF and LMF performed in a cell-free assay. The small number of antioxidant system parameters measured did not allow detecting differences between HMF and LMF.
Insights
Hydrogen peroxide (H₂O₂) causes oxidative damage in human placental mitochondria (LMF and HMF). The antioxidant systems in both mitochondrial fractions responded similarly to H₂O₂ exposure.
Area of Science:
- Mitochondrial biochemistry
- Human placental research
- Oxidative stress biology
Background:
- Human placenta contains two distinct mitochondrial fractions: light (LMF) and heavy (HMF).
- Mitochondria are primary sources of reactive oxygen species (ROS).
- Mitochondrial dysfunction and oxidative stress pose risks to placental health and fetal development.
Purpose of the Study:
- To assess the antioxidant capacity of placental LMF and HMF.
- To determine the susceptibility of placental LMF and HMF to oxidative stress.
Main Methods:
- Isolated human placental mitochondrial fractions (LMF and HMF) from healthy donors.
- Incubation of MFs with hydrogen peroxide (H₂O₂).
- Measurement of catalase (CAT) activity, reduced glutathione (GSH), lipid peroxidation (LP), and protein carbonylation (PC).
Main Results:
- H₂O₂ exposure increased lipid peroxidation and protein carbonylation.
- H₂O₂ treatment decreased catalase activity.
- Reduced glutathione levels remained unchanged after H₂O₂ treatment in both LMF and HMF.
Conclusions:
- Hydrogen peroxide induces oxidative damage in both light and heavy mitochondrial fractions of the human placenta.
- The measured antioxidant systems in LMF and HMF exhibited similar responses to oxidative stress.
- This study provides initial insights into placental mitochondrial antioxidant defense, though further parameters are needed to differentiate HMF and LMF responses.
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