ArticleChemico-biological interactions2016
Developmental expression of paraoxonase 2.
Article in Chemico-biological interactions, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- FOXA1 Suppresses Endoplasmic Reticulum Stress, Oxidative Stress, and Neuronal Apoptosis in Parkinson's Disease by Activating PON2 Transcription.Neurotoxicity research · 2024Article
- Paraoxonases at the Heart of Neurological Disorders.International journal of molecular sciences · 2023Review
- Examining the role of paraoxonase 2 in the dopaminergic system of the mouse brain.BMC neuroscience · 2022Article
- Pioglitazone transiently stimulates paraoxonase-2 expression in male nonhuman primate brain: Implications for sex-specific therapeutics in neurodegenerative disorders.Neurochemistry international · 2022Article
- Expression of PON2 isoforms varies among brain regions in male and female African green monkeys.Free radical biology & medicine · 2022Article
- Insights into the role of paraoxonase 2 in human pathophysiology.Journal of biosciences · 2022Article
- Sex-based disparity in paraoxonase-2 expression in the brains of African green monkeys.Free radical biology & medicine · 2021Article
- PPARγ/PGC1α signaling as a potential therapeutic target for mitochondrial biogenesis in neurodegenerative disorders.Pharmacology & therapeutics · 2021Review
- Paraoxonase Role in Human Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2020Review
- Parkinson's disease treatment: past, present, and future.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- Pioglitazone activates paraoxonase-2 in the brain: A novel neuroprotective mechanism.Experimental neurology · 2020Article
- Paraoxonases Activities and Polymorphisms in Elderly and Old-Age Diseases: An Overview.Antioxidants (Basel, Switzerland) · 2019Review
- Paraoxonase-2 variants potentially influence insulin resistance, beta-cell function, and their interrelationships with alanine aminotransferase in type 2 diabetes.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2018Article
- Sex and genetic differences in the effects of acute diesel exhaust exposure on inflammation and oxidative stress in mouse brain.Toxicology · 2016Article
- Paraoxonases-1, -2 and -3: What are their functions?Chemico-biological interactions · 2016Article
- Paraoxonase 2 deficiency in mice alters motor behavior and causes region-specific transcript changes in the brain.Neurotoxicology and teratologyArticle
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Paraoxonase 2 (PON2) is a member of the paraoxonase gene family also comprising PON1 and PON3. PON2 functions as a lactonase and exhibits anti-bacterial as well as antioxidant properties. At the cellular level, PON2 localizes to the mitochondrial and endoplasmic reticulum membranes where it scavenges reactive oxygen species. PON2 is of particular interest as it is the only paraoxonase expressed in brain tissue and appears to play a critical role in mitigating oxidative stress in the brain. The aim of this study was to investigate the expression of PON2 at the protein and mRNA level in the brain and liver of mice through development to identify potential age windows of susceptibility to oxidative stress, as well as to compare expression of hepatic PON2 to expression of PON1 and PON3. Overall, PON2 expression in the brain was lower in neonatal mice and increased with age up to postnatal day (PND) 21, with a significant decrease observed at PND 30 and 60. In contrast, the liver showed continuously increasing levels of PON2 with age, similar to the patterns of PON1 and PON3. PON2 protein levels were also investigated in brain samples from non-human primates, with PON2 increasing with age up to the infant stage and decreasing at the juvenile stage, mirroring the results observed in the mouse brain. These variable expression levels of PON2 suggest that neonatal and young adult animals may be more susceptible to neurological insult by oxidants due to lower levels of PON2 in the brain.
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