The DOI matches its Crossref record; 47 of the 47 references it cites were found in a registry or an index.
Paraoxonase Status in Coronary Heart Disease: Are Activity and Concentration More Important Than Genotype?
Abstract
Human serum paraoxonase (PON1) hydrolyzes oxidized lipids in low density lipoprotein (LDL) and could therefore retard the development of atherosclerosis. In keeping with this hypothesis, several case-control studies have shown a relationship between the presence of coronary heart disease (CHD) and polymorphisms at amino acid positions 55 and 192 of PON1, which we associated with a decreased capacity of PON1 to protect LDL against the accumulation of lipid peroxides, but some other studies have not. However, the PON1 polymorphisms are only 1 factor in determining the activity and concentration of the enzyme. Only 3 of the previous 18 studies directly determined PON1 activity and concentration. Therefore, we studied PON1 activity, concentration, and gene distribution in 417 subjects with angiographically proven CHD and in 282 control subjects. We found that PON1 activity and concentration were significantly lower in subjects with CHD than in control subjects (activity to paraoxon 122.8 [3.3 to 802.8] versus 214.6 [26.3 to 620.8] nmol · min −1 · mL −1 , P <0.001; concentration 71.6 [11.4 to 489.3] versus 89.1 [16.8 to 527.4] μg/mL, P <0.001). There were no differences in the PON1-55 and -192 polymorphisms or clusterin concentration between patients with CHD and control subjects. These results indicate that lower PON1 activity and concentration and, therefore, the reduced ability to prevent LDL lipid peroxidation may be more important in determining the presence of CHD than paraoxonase genetic polymorphisms.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Bias in meta-analysis detected by a simple, graphical test
Egger, M., Smith, G. D., Schneider, M., & Minder, C. (1997) · BMJ · doi:10.1136/bmj.315.7109.629 · Cited by 56,722
Meta-analysis in clinical trials
DerSimonian, R., & Laird, N. (1986) · Controlled Clinical Trials · doi:10.1016/0197-2456(86)90046-2 · Cited by 39,552
Epstein, F. H., Steinberg, D., Parthasarathy, S., Carew, T. E., Khoo, J. C., & Witztum, J. L. (1989) · New England Journal of Medicine · doi:10.1056/nejm198904063201407 · Cited by 6,427
Watson, A. D., Berliner, J. A., Hama, S. Y., La Du, B. N., Faull, K. F., Fogelman, A. M., & Navab, M. (1995) · Journal of Clinical Investigation · doi:10.1172/jci118359 · Cited by 1,154
Mice lacking serum paraoxonase are susceptible to organophosphate toxicity and atherosclerosis
Shih, D. M., Gu, L., Xia, Y.-R., Navab, M., Li, W.-F., Hama, S., Castellani, L. W., Furlong, C. E., Costa, L. G., Fogelman, A. M., et al. (1998) · Nature · doi:10.1038/28406 · Cited by 1,078
Paraoxonase prevents accumulation of lipoperoxides in low‐density lipoprotein
Mackness, M. I., Arrol, S., & Durrington, P. N. (1991) · FEBS Letters · doi:10.1016/0014-5793(91)80962-3 · Cited by 977
Self-citationThe molecular basis of the human serum paraoxonase activity polymorphism
Humbert, R., Adler, D. A., Disteche, C. M., Hassett, C., Omiecinski, C. J., & Furlong, C. E. (1993) · Nature Genetics · doi:10.1038/ng0193-73 · Cited by 841
Van Lenten, B. J., Hama, S. Y., de Beer, F. C., Stafforini, D. M., McIntyre, T. M., Prescott, S. M., La Du, B. N., Fogelman, A. M., & Navab, M. (1995) · Journal of Clinical Investigation · doi:10.1172/jci118345 · Cited by 840
High-density lipoprotein inhibits the oxidative modification of low-density lipoprotein
Parthasarathy, S., Barnett, J., & Fong, L. G. (1990) · Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism · doi:10.1016/0005-2760(90)90314-n · Cited by 827
MACKNESS, M., ARROL, S., ABBOTT, C., & DURRINGTON, P. (1993) · Atherosclerosis · doi:10.1016/0021-9150(93)90183-u · Cited by 816
Self-citation
Cited by
Oxidative Stress and Vascular Disease
Madamanchi, N. R., Vendrov, A., & Runge, M. S. (2005) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/01.atv.0000150649.39934.13 · Cited by 1,618
Bhattacharyya, T. (2008) · JAMA · doi:10.1001/jama.299.11.1265 · Cited by 533
Oxidative stress and atherosclerosis
Singh, U., & Jialal, I. (2006) · Pathophysiology · doi:10.1016/j.pathophys.2006.05.002 · Cited by 490
Metadata
- Authors
- Mackness, B., Davies, G. K., Turkie, W., Lee, E., Roberts, D. H., Hill, E., Roberts, C., Durrington, P. N., & Mackness, M. I.
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2001-09
- Volume
- 21
- Issue
- 9
- Pages
- 1451-1457
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2159959895
- Cited by
- 435
- References
- 47
- FWCI
- 12.62
- Type
- journal article
- Language
- en
- Open access
- closed
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: Paraoxonase Status in Coronary Heart Disease: Are Activity and Concentration More Important Than Genotype? https://app.cochat.ai/papers/10.1161/hq0901.094247
- The paper
- Mackness, B., Davies, G. K., Turkie, W., Lee, E., Roberts, D. H., Hill, E., Roberts, C., Durrington, P. N., & Mackness, M. I. (2001). Paraoxonase Status in Coronary Heart Disease: Are Activity and Concentration More Important Than Genotype? Arteriosclerosis, Thrombosis, and Vascular Biology. https://doi.org/10.1161/hq0901.094247
Data sources
Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.