ArticleFrontiers in neuroscience2017
NADPH Oxidase Isoform 2 (NOX2) Is Involved in Drug Addiction Vulnerability in Progeny Developmentally Exposed to Ethanol.
Article in Frontiers in neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 30 citations in OpenAlex.
- Developmental origins and environmental determinants of cardiovascular-kidney-metabolic syndrome: A pediatric precision prevention perspective.Biomedical journal · 2026Review
- Resveratrol and Redox Regulation in Cardiovascular Disease Across the Life Course: Mechanistic and Translational Perspectives.Antioxidants (Basel, Switzerland) · 2026Review
- Impact of Maternal High-Fat Diet on Offspring Cardiovascular-Kidney-Metabolic Health: Spotlight on Oxidative Stress.Antioxidants (Basel, Switzerland) · 2025Review
- Early-Life Prevention of Cardiovascular-Kidney-Metabolic Syndrome: The DOHaD Perspective on Resveratrol and Short-Chain Fatty Acids.Antioxidants (Basel, Switzerland) · 2025Review
- Animal Models for Studying Developmental Origins of Cardiovascular-Kidney-Metabolic Syndrome.Biomedicines · 2025Review
- Decreased antioxidant-related superoxide dismutase 1 expression in peripheral immune cells indicates early ethanol exposure.Scientific reports · 2024Article
- Exercise reduces physical alterations in a rat model of fetal alcohol spectrum disorders.Biological research · 2024Article
- Alginate Oligosaccharides Protect Gastric Epithelial Cells against Oxidative Stress Damage through Induction of the Nrf2 Pathway.Antioxidants (Basel, Switzerland) · 2024Article
- Nutritional Approaches Targeting Gut Microbiota in Oxidative-Stress-Associated Metabolic Syndrome: Focus on Early Life Programming.Nutrients · 2024Review
- Melatonin Use during Pregnancy and Lactation Complicated by Oxidative Stress: Focus on Offspring's Cardiovascular-Kidney-Metabolic Health in Animal Models.Antioxidants (Basel, Switzerland) · 2024Review
- Irisin attenuates ethanol-induced behavioral deficits in mice through activation of Nrf2 and inhibition of NF-κB pathways.Metabolic brain disease · 2023Article
- Article
- Metabolic Syndrome Programming and Reprogramming: Mechanistic Aspects of Oxidative Stress.Antioxidants (Basel, Switzerland) · 2022Review
- Prenatal Ethanol Exposure Misregulates Genes Involved in Iron Homeostasis Promoting a Maladaptation of Iron Dependent Hippocampal Synaptic Transmission and Plasticity.Frontiers in pharmacology · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ethanol exposure increases oxidative stress in developing organs, including the brain. Antioxidant treatment during maternal ethanol ingestion improves behavioral deficits in rodent models of fetal alcohol spectrum disorder (FASD). However, the impact of general antioxidant treatment in their adult offspring and the Specific Reactive Species (ROS)-dependent mechanism, are not fully understood. We hypothesized that pre and early postnatal ethanol exposure (PEE) modifies redox homeostasis, in particular NOX2 function during reward signaling in the mesocorticolimbic pathway, which reinforces the effects of alcohol. We developed a FASD rat model which was evaluated during adolescence (P21) and adulthood (P70). We first studied whether redox homeostasis is affected in PEE animals, by analyzing mRNA expression of SOD1, CAT, and Gpx1. We found that PEE reduced the mRNA levels of these three anti-oxidant enzymes in PFC and HIPP at P21 and in the VTA at P70. We also analyzed basal mRNA and protein expression of NOX2 subunits such as gp91phox, p22 phox, and p47 phox, in mesocorticolimbic brain areas of PEE rat brains. At P21, gp91 phox, and p47 phox levels in the VTA were decreased. At P70, gp91 phox mRNA levels was decreased in HIPP and both mRNA and protein levels were decreased in PFC. Since NOX2 is regulated by the N-methyl-D-aspartate Receptor (NMDAR), we analyzed NMDAR mRNA expression and found differential expression of NMDAR subunits (NR1 and NR2B) in the PFC that was age dependent, with levels decreased at P21 and increased at P70. The analysis also revealed decreased NR2B mRNA expression in HIPP and VTA at P70. Offspring from maternal ethanol users consumed 25% more ethanol in a free choice alcohol consumption test than control rats, and showed place preference for an alcohol-paired compartment.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.