Ask about this productRelated genes to: PON1 antibody
- Gene:
- PON1 NIH gene
- Name:
- paraoxonase 1
- Previous symbol:
- PON
- Synonyms:
- ESA
- Chromosome:
- 7q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2014-11-19
Related products to: PON1 antibody
Related articles to: PON1 antibody
- Mercury is among the worst global pollutants being a significant public health concern in the Amazon, primarily due to contaminated fish intake. The relationship between mercury body burden and genetic polymorphisms in GSTP1 (rs1695), PON1 (rs662), MT1A (rs11076161), and SEPP1 (rs7579) genes was analyzed in Amazonian riverine populations, with a rapid and cost-effective approach by selecting individuals at both extremes of the exposure spectrum. Genotyping revealed significant associations for GSTP1 and PON1 polymorphisms: the G allele of GSTP1 and the CC genotype of PON1 were more frequent among highly exposed individuals, suggesting reduced detoxification efficiency. Additionally, although non-significant, a higher prevalence of the GG and CC genotypes were observed for MT1A and SEPP1, respectively, in the high-exposure group, pointing to the need for further investigation. These findings enhance our understanding of how genetic variation influences individual susceptibility to mercury accumulation in the Amazon and can support public health prevention strategies and the early identification of high-risk individuals within these vulnerable populations. Furthermore, this study underscores the importance of considering gene-environment interactions in environmental health assessments and highlights the need for public health strategies tailored to the genetic and socio-environmental contexts of vulnerable Amazonian communities. - Source: PubMed
Publication date: 2026/08/14
Lopes-Araújo AmandaBarthelemy Jean LudgerArrifano Gabriela PSantos-Sacramento LetíciaSoares-Silva IsabelaLeal-Nazaré Caio GLago-Pinheiro CamilaMacchi Barbarella MMartín-Doimeadios Rosa C RodríguezJiménez-Moreno MaríaAugusto-Oliveira MarcusCrespo-López Maria Elena - Oxidative stress and systemic inflammation are considered key mechanisms linking obstructive sleep apnea (OSA) to cardiovascular disease. This study aimed to investigate the relationships among oxidative stress, nitrosative stress, inflammatory biomarkers, and echocardiographic alterations in OSA. This cross-sectional observational study included 72 adults with OSA, classified according to disease severity as mild, moderate, or severe. Clinical characteristics and echocardiographic parameters were assessed. Oxidative stress biomarkers-malondialdehyde (MDA), total oxidant status (TOS), total antioxidant capacity (TAC), nitric oxide (NO), oxidative stress index (OSI), and paraoxonase-1 (PON1); the nitrosative stress marker 3-nitrotyrosine (3-NT), inflammatory biomarkers-interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α); and N-terminal pro-B-type natriuretic peptide (NT-proBNP)-were determined using spectrophotometric and ELISA methods. Correlation and regression analyses were performed to evaluate associations between oxidative stress and inflammation. No significant differences in echocardiographic parameters, oxidative stress biomarkers, inflammatory markers, or NT-proBNP concentrations were observed across OSA severity categories (all > 0.05). Patients with diabetes mellitus exhibited larger left and right atrial diameters and higher pulmonary artery systolic pressure values compared with non-diabetic patients (all < 0.05). Significant positive correlations were identified between IL-6 and MDA (ρ = 0.364, = 0.002), TOS (ρ = 0.259, = 0.029), and OSI (ρ = 0.257, = 0.030). The nitrosative stress marker 3-NT was also positively correlated with MDA, TOS, and OSI (all < 0.05). In multivariable regression analyses adjusted for age, body mass index, and diabetes mellitus, MDA remained independently associated with IL-6 concentrations (B = 1.776, 95% CI 0.110-3.442, standardized β = 0.271, = 0.037). Similarly, OSI remained independently associated with IL-6 (B = 0.043, 95% CI 0.003-0.083, standardized β = 0.277, = 0.034). OSA severity was not associated with significant differences in oxidative stress, inflammatory, or echocardiographic parameters. However, oxidative stress biomarkers were strongly interrelated and remained significantly associated with IL-6 concentrations, suggesting a potential link between oxidative stress and systemic inflammation in patients with OSA. These findings support further investigation of oxidative stress pathways as biomarkers of disease-related biological activity in OSA. - Source: PubMed
Publication date: 2026/08/01
Zinveliu Bercian Crina VeronicaMăgureanu Dan ClaudiuPop Raluca MariaSitar-Tăut Adela-VivianaCozma AngelaOrășan Olga HildaLucaciu Roxana LianaHangan Adriana CorinaProcopciuc Lucia Maria - Research has found that paraoxonase 1 (PON1) is closely related to cardiovascular disease, but the relationship between circulating PON1 levels and coronary artery stenosis (CAS) in patients with diabetes remains unclear. - Source: PubMed
Publication date: 2026/07/27
Zhao YuWang YanMao LinZeng XiangjunYang LongyanZhao Dong - This study aimed to investigate the molecular detection of Anaplasma spp. in sheep from the Northeastern Anatolia region of Türkiye and to evaluate the effects of infection on oxidative stress, antioxidant protection, and inflammation. - Source: PubMed
Publication date: 2026/08/01
Başer LaleAydin Nilgün - Metabolic plasticity driven by mitochondrial oxidative phosphorylation (OXPHOS) is increasingly recognized as a key determinant of therapeutic tolerance in hepatocellular carcinoma (HCC), but the upstream regulators that preserve electron transport chain stability during treatment remain poorly defined. In this study, we identified paraoxonase-1 (PON1) as a clinically relevant regulator of mitochondrial metabolism and lenvatinib response in HCC. PON1 was markedly upregulated in HCC and independently associated with poor overall and recurrence-free survival. Functionally, PON1 promoted tumor growth and conferred robust tolerance to lenvatinib. Mechanistically, PON1 directly interacted with and stabilized NDUFA4, a key component required for complex IV assembly, thereby maintaining mitochondrial membrane potential, complex IV integrity, and OXPHOS-dependent adenosine triphosphate production while limiting reactive oxygen species accumulation. Genetic silencing of PON1 or NDUFA4 impaired mitochondrial respiration, increased oxidative stress, and restored lenvatinib sensitivity in HCC cells and xenograft models. Structure-guided virtual screening identified the Food and Drug Administration-approved CFTR corrector lumacaftor as a potent modulator of PON1 that disrupted the PON1-NDUFA4 interaction and enhanced the antitumor efficacy of lenvatinib in vivo. These findings identify the PON1-NDUFA4 axis as a previously unrecognized metabolic vulnerability that sustains mitochondrial respiratory fitness and lenvatinib resistance in HCC. Targeting mitochondrial protein-stabilizing mechanisms such as PON1-NDUFA4 may offer a broadly applicable strategy for overcoming therapy resistance in liver cancer and other aggressive malignancies. Implications: These findings establish mitochondrial protein stabilization as an actionable therapeutic vulnerability and provide a rationale for combination strategies to overcome targeted therapy resistance in HCC. - Source: PubMed
Publication date: 2026/07/28
Lin Shi-LinWang YueZheng Yi-MinKe Ai-WuMa A-YingGao Chao