Susceptibility of placental mitochondria to oxidative stress

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 repre...

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Autores principales: Papa Gobbi, R., Magnarelli, G., Rovedatti, M.G.
Formato: JOUR
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Acceso en línea:http://hdl.handle.net/20.500.12110/paper_24721727_v110_n16_p1228_PapaGobbi
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spelling todo:paper_24721727_v110_n16_p1228_PapaGobbi2023-10-03T16:42:27Z Susceptibility of placental mitochondria to oxidative stress Papa Gobbi, R. Magnarelli, G. Rovedatti, M.G. mitochondria oxidative stress placenta reactive oxygen species catalase glutathione hydrogen peroxide malonaldehyde adult antioxidant activity Article cell isolation controlled study enzymatic assay enzyme activity female human human tissue lipid peroxidation mitochondrion normal human oxidation oxidative stress placenta protein carbonylation protein determination spectrophotometry 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 H2O2. Catalase (CAT) activity, and reduced glutathione (GSH), lipid peroxidation (LP), and protein carbonylation (PC) levels were determined. Results: H2O2 treatment increased LP and PC levels and decreased CAT activity. GSH levels were similar in control and treated MFs. Conclusion: H2O2 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. © 2018 Wiley Periodicals, Inc. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_24721727_v110_n16_p1228_PapaGobbi
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic mitochondria
oxidative stress
placenta
reactive oxygen species
catalase
glutathione
hydrogen peroxide
malonaldehyde
adult
antioxidant activity
Article
cell isolation
controlled study
enzymatic assay
enzyme activity
female
human
human tissue
lipid peroxidation
mitochondrion
normal human
oxidation
oxidative stress
placenta
protein carbonylation
protein determination
spectrophotometry
spellingShingle mitochondria
oxidative stress
placenta
reactive oxygen species
catalase
glutathione
hydrogen peroxide
malonaldehyde
adult
antioxidant activity
Article
cell isolation
controlled study
enzymatic assay
enzyme activity
female
human
human tissue
lipid peroxidation
mitochondrion
normal human
oxidation
oxidative stress
placenta
protein carbonylation
protein determination
spectrophotometry
Papa Gobbi, R.
Magnarelli, G.
Rovedatti, M.G.
Susceptibility of placental mitochondria to oxidative stress
topic_facet mitochondria
oxidative stress
placenta
reactive oxygen species
catalase
glutathione
hydrogen peroxide
malonaldehyde
adult
antioxidant activity
Article
cell isolation
controlled study
enzymatic assay
enzyme activity
female
human
human tissue
lipid peroxidation
mitochondrion
normal human
oxidation
oxidative stress
placenta
protein carbonylation
protein determination
spectrophotometry
description 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 H2O2. Catalase (CAT) activity, and reduced glutathione (GSH), lipid peroxidation (LP), and protein carbonylation (PC) levels were determined. Results: H2O2 treatment increased LP and PC levels and decreased CAT activity. GSH levels were similar in control and treated MFs. Conclusion: H2O2 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. © 2018 Wiley Periodicals, Inc.
format JOUR
author Papa Gobbi, R.
Magnarelli, G.
Rovedatti, M.G.
author_facet Papa Gobbi, R.
Magnarelli, G.
Rovedatti, M.G.
author_sort Papa Gobbi, R.
title Susceptibility of placental mitochondria to oxidative stress
title_short Susceptibility of placental mitochondria to oxidative stress
title_full Susceptibility of placental mitochondria to oxidative stress
title_fullStr Susceptibility of placental mitochondria to oxidative stress
title_full_unstemmed Susceptibility of placental mitochondria to oxidative stress
title_sort susceptibility of placental mitochondria to oxidative stress
url http://hdl.handle.net/20.500.12110/paper_24721727_v110_n16_p1228_PapaGobbi
work_keys_str_mv AT papagobbir susceptibilityofplacentalmitochondriatooxidativestress
AT magnarellig susceptibilityofplacentalmitochondriatooxidativestress
AT rovedattimg susceptibilityofplacentalmitochondriatooxidativestress
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