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
- Atherosclerosis, a chronic inflammatory disease driven by lipid metabolism disorders and oxidative stress, remains a leading cause of mortality. Statins are effective but have significant side effects, necessitating exploration of safer herbal alternatives. Prosopis farcta and Scrophularia striata are two flavonoid-rich plants traditionally used for cardiac pain. The present study aims to compare the effects of extracts of these plants along with related parameters in male Wistar rats fed a High-Cholesterol Diet (HCD). - Source: PubMed
Publication date: 2026/09/11
Gharibi AghdasHeidarizadi SomayehAbbasi NaserHeidarbaigi KhadijehAzizi Monireh - Rheumatoid arthritis (RA) is characterized by inflammation and an increased risk for cardiovascular disease. Although it is known that metabolic disturbances alter macrophage metabolism, inflammatory responses and the ability to maintain immune homeostasis, these changes have not been well studied out of the context of atherosclerosis. Our aim was to investigate the effect of dyslipidemia caused by ApoE deficiency on macrophages and on antigen-induced arthritis in mice. Toward this aim, mice deficient in the ApoE gene were used which exhibit high total cholesterol (TC) levels distributed primarily in VLDL/IDL fractions, normal triglycerides and low HDL-C levels associated with distribution at lower densities and lower PON-1 activity. ApoE KO peritoneal macrophages had an M1-like polarization and an increased respiration rate. Importantly, ApoE KO mice developed more severe knee joint swelling compared to control mice. At the end of the arthritis protocol, spleen macrophages had increased expression of M1 cell surface markers. Simvastatin treatment reduced serum TC, increased HDL-C and PON-1 activity and improved HDL density. Additionally, treatment of ApoE KO mice with simvastatin limited the M1-associated cell surface markers on spleen macrophages and reduced arthritic joint swelling. Collectively, our findings support further investigation of lipid-modifying strategies in the context of inflammatory arthritis associated with dyslipidemia. - Source: PubMed
Publication date: 2026/09/19
Kakale AsiminaLazaridou DespoinaAxiotis IsidorosTzardi MariaKardassis Dimitris - High-density lipoproteins (HDL) are essential to alleviate the progression of atherosclerosis by mediating reverse-cholesterol transport, antioxidant and anti-inflammatory effects. We aimed to enhance the expression of endogenous HDL components, apolipoprotein A1 (APOA1) and antioxidant enzyme paraoxonase 1 (PON1), and to investigate their athero-protective effects. The CRISPR/dCas9 technology was used to activate the transcription of endogenous APOA1/PON1 in human hepatocytes (Huh7 line) and Apoa1/Pon1 in apoE mice. The expression of APOA1/PON1 genes was successfully upregulated in hepatocytes, and their proteins were secreted in the culture medium in the presence/absence of tumor necrosis factor-α (TNFα). APOA1-rich Huh7-derived conditioned medium exerted antioxidant and anti-inflammatory effects in TNFα-activated EA.hy926 endothelial cells. A single dose of the CRISPR/dCas9 plasmids i.v. injected in apoE mice increased the expression of hepatic Apoa1/Pon1 and their serum levels up to four weeks. FPLC analysis showed that increased serum APOA1 was distributed between HDL, LDL, and in lipid-free form. These mice also exhibited high levels of hepatic, gallbladder and feces cholesterol, in part due to the upregulation of hepatic scavenger receptor class-B1, cholesterol 7-alpha-hydroxylase, and ATP-binding cassette sub-family-G-member-8 transporter. In apoE mice with upregulated Apoa1/Pon1, no increased inflammatory stress or innate immune activation were detected, while lipid peroxides were decreased in PON1 mice. Of major interest, the area of aortic lipid deposits was halved in the treated mice. Our findings demonstrate the successful upregulation of endogenous Apoa1/Pon1 in apoE mice by using the CRISPR/dCas9 system, and highlight new mechanisms for APO1/PON1 anti-atherosclerotic action, explaining the reduction of aortic lipid deposits. - Source: PubMed
Publication date: 2026/09/18
Toma LauraBarbălată TeodoraHărătău Jessica Isabela CătălinaSanda Gabriela MariaFuior Elena ValeriaFenyo Ioana MădălinaNiculescu Loredan ŞtefanDăian Laura-MariaSasson ShlomoSima Anca VolumniaStancu Camelia Sorina - Chronic lead (Pb) exposure is a recognized cardiovascular toxicant, however its long-term impact on HDL-associated antioxidant defenses and genetic susceptibility remains unclear. Paraoxonase-1 (PON1), an HDL-bound enzyme, limits lipid peroxidation and atherogenic modification. We conducted a 3-year longitudinal study of 141 Pb workers with repeated measures of blood lead (B-Pb), serum lipids, and PON1 activities (arylesterase, paraoxonase, diazoxonase). PON1 Q192R, L55M, and C108T polymorphisms were genotyped. Generalized estimating equation models adjusted for demographic, occupational, and behavioral factors. Higher B-Pb levels were consistently associated with reduced HDL-C-adjusted arylesterase, diazoxonase and paraoxonase activities. Each 1 µg/dL increase in B-Pb corresponded to a 0.0093 µmol/min/mL× [HDL] decrease in arylesterase activity (p < 0.001). Although genotypes influenced baseline enzyme levels, no significant gene-lead interaction was observed. These findings indicate that chronic Pb exposure suppresses PON1 antioxidant function independently of these genetic variants, supporting HDL dysfunction as a mechanistic link between Pb exposure and cardiovascular toxicity. - Source: PubMed
Publication date: 2026/09/14
Luo Kuei-HauYeh Chen-LingYang Chen-ChengChuang Hung-Yi - Exposure to agricultural pesticides has been suggested as a potential environmental risk factor for hematological malignancies. However, evidence regarding the relationship between pesticide exposure, oxidative stress, and acute leukemia remains limited in high-exposure agricultural regions. This study aimed to investigate the association between organochlorine pesticide exposure and oxidative stress biomarkers in patients with acute leukemia in Kerman Province, Iran. In this case-control study, 72 patients diagnosed with acute leukemia and 72 healthy controls were enrolled. Serum concentrations of organochlorine pesticides were measured using gas chromatography. Oxidative stress biomarkers, including malondialdehyde (MDA) and total antioxidant capacity (TAC), as well as pesticide toxicity/exposure biomarkers, including acetylcholinesterase (AChE), and paraoxonase-1 (PON1), were evaluated. Statistical analyses were performed using independent t-tests, correlation analysis, logistic regression, and survival models. Patients with acute leukemia showed significantly higher serum levels of organochlorine pesticides compared with controls ( < 0.001). Oxidative stress markers were significantly altered in the patient group, with increased MDA levels and reduced TAC levels. In addition, AChE and PON1 activities were significantly lower among patients than controls ( < 0.001). Positive correlations were observed between pesticide exposure and oxidative stress indices. Multivariate logistic regression analysis identified pesticide exposure as an independent factor associated with hematological malignancies (OR = 3.5, 95% CI: 2.2-5.4). The findings suggest that chronic exposure to agricultural pesticides may contribute to oxidative stress imbalance and impaired detoxification capacity in patients with acute leukemia. These results highlight the importance of environmental exposure monitoring and preventive strategies in agricultural communities with high pesticide use. - Source: PubMed
Publication date: 2026/09/11
Kashani MostafaKarimi Darabi MehrnazRafeeinia Arash