Neurodevelopmental damage after prenatal infection: role of oxidative stress in the fetal brain

Lanté, Fabien; Meunier, Johann; Guiramand, Janique; Maurice, Tangui; Cavalier, Mélanie; de Jesus Ferreira, Marie-Céleste; Aimar, Rose; Cohen-Solal, Catherine; Vignes, Michel; Barbanel, Gérard

doi:10.1016/j.freeradbiomed.2007.01.027

Cited by 140Neonatal and fetal brain pathologyAnesthesia and Neurotoxicity ResearchTryptophan and brain disorders

Neurodevelopmental damage after prenatal infection: role of oxidative stress in the fetal brain

Lanté, Fabien, Meunier, Johann, Guiramand, Janique, Maurice, Tangui, Cavalier, Mélanie, de Jesus Ferreira, Marie-Céleste, Aimar, Rose, Cohen-Solal, Catherine +2 more·2007·Free Radical Biology and Medicine

DOI 10.1016/j.freeradbiomed.2007.01.027

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Abstract

Prenatal infection is a major risk responsible for the occurrence of psychiatric conditions in infants. Mimicking maternal infection by exposing pregnant rodents to bacterial endotoxin lipopolysaccharide (LPS) also leads to major brain disorders in the offspring. The mechanisms of LPS action remain, however, unknown. Here, we show that LPS injection during pregnancy in rats, 2 days before delivery, triggered an oxidative stress in the hippocampus of male fetuses, evidenced by a rapid rise in protein carbonylation and by decreases in alpha-tocopherol levels and in the ratio of reduced/oxidized forms of glutathione (GSH/GSSG). Neither protein carbonylation increase nor decreases in alpha-tocopherol levels and GSH/GSSG ratio were observed in female fetuses. NMDA synaptic currents and long-term potentiation in CA1, as well as spatial recognition in the water maze, were also impaired in male but not in female 28-day-old offspring. Pretreatment with the antioxidant N-acetylcysteine prevented the LPS-induced changes in the biochemical markers of oxidative stress in male fetuses, and the delayed detrimental effects in male 28-day-old offspring, completely restoring both long-term potentiation in the hippocampus and spatial recognition performance. Oxidative stress in the hippocampus of male fetuses may thus participate in the neurodevelopmental damage induced by a prenatal LPS challenge.

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Such augmented disruption occurs via activation of cellular redox signaling in response to infection.
“Such augmented disruption occurs via the activation of the cellular redox signaling in response to infection [130,133].”
From The ASD Living Biology: from cell proliferation to clinical phenotype (2019) · cites this paper as [133]
The deleterious effect of early-life immune challenge on parvalbumin interneurons could result from redox dysregulation, as maternal immune challenge transiently decreases glutathione and vitamin E levels and increases oxidative stress in the hippocampus.
“This deleterious effect could result from a redox dysregulation as maternal immune challenge transiently decreases GSH and vitamin E levels and increase oxidative stress in the hippocampus (Lante et al., 2007).”
From Redox dysregulation, neuroinflammation, and NMDA receptor hypofunction: A “central hub” in schizophrenia pathophysiology? (2016) · cites this paper as Lante et al., 2007

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Authors: Lanté, F., Meunier, J., Guiramand, J., Maurice, T., Cavalier, M., de Jesus Ferreira, M.-C., Aimar, R., Cohen-Solal, C., Vignes, M., & Barbanel, G.
Affiliations: Centre National de la Recherche Scientifique (FR)
Corresponding author: Barbanel, Gérard
ORCID: Lanté, Fabien
Meunier, Johann
Guiramand, Janique
Maurice, Tangui
Vignes, Michel
Venue: Free Radical Biology and Medicine
Publisher: Elsevier BV
Published: 2007-04
Volume: 42
Issue: 8
Pages: 1231-1245
ISSN: 0891-5849 (ISSN-L)
DOI: 10.1016/j.freeradbiomed.2007.01.027
OpenAlex: W1987843838
Cited by: 140
References: 77
Citations by year: 2026: 5 · 2025: 2 · 2024: 6 · 2023: 7 · 2022: 4 · 2021: 6 · 2020: 5 · 2019: 6 · 2018: 7 · 2017: 7 · 2016: 12 · 2015: 16 · 2014: 10 · 2013: 9 · 2012: 14
FWCI: 5.36
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
Locations: Free Radical Biology and Medicine (publishedVersion)
PubMed (publishedVersion)
HAL (submittedVersion)
Topics: Health Sciences › Medicine › Pediatrics, Perinatology and Child Health › Neonatal and fetal brain pathology
Life Sciences › Neuroscience › Developmental Neuroscience › Anesthesia and Neurotoxicity Research
Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords: prenatal infection, lipopolysaccharide, oxidative stress, fetal hippocampus, neurodevelopmental damage, protein carbonylation, alpha-tocopherol, glutathione, long-term potentiation, spatial recognition, sex differences, N-acetylcysteine, maternal infection, rodent models
MeSH terms: Animals, Brain, Brain Diseases, Chromatography, High Pressure Liquid, Female, Glutathione, Hippocampus, Infections, Lipopolysaccharides, Pregnancy, Rats, Sprague-Dawley, Oxidative Stress, Patch-Clamp Techniques, Glutathione Disulfide, alpha-Tocopherol, Rats

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Neurodevelopmental damage after prenatal infection: role of oxidative stress in the fetal brain

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