Objectives: Prolidase is a cytosolic exopeptidase that cleaves iminodipeptides with carboxy-terminal proline or hydroxyproline and plays major role in collagen turnover. Collagen is the essential content in atherosclerotic plaque playing a key role in the stability/instability of and progression of coronary artery disease (CAD). Consequently, in this study we sought to determine serum prolidase activity and markers of oxidative stress such as lipid hydroperoxide and total free sulfhydryl in CAD.
Design And Methods: We have evaluated 199 patients with CAD and 122 control cases with clinical, electrocardiographic, and laboratory investigation. We have measured serum prolidase activity and serum total free sulfhydryl levels spectrophotometrically. Serum lipid hydroperoxide levels were determined with ferrous ion oxidation-xylenol orange method. We assessed the association of serum prolidase activity with the presence and severity of CAD and clinical characteristics, and laboratory parameters.
Results: Serum prolidase activity (52.5+/-5.6 vs. 46.7+/-5.1 U/l, respectively, P<0.001) and serum lipid hydroperoxide levels were significantly increased in patients with CAD compared with control cases whereas, serum total free sulfhydryl levels were significantly decreased in patients with CAD compared with control cases. Serum prolidase activity and total free sulfhydryl levels were independent predictors of the presence of CAD [(chi=75.532, ss=0.212, P=0.003) and (chi=25.969, ss=-30.486, P=0.019), respectively] and Gensini score [(beta=0.276, P<0.001) and (beta=-0.274, P<0.001), respectively]. Independent predictors of serum prolidase activity were serum high-density lipoprotein cholesterol (beta=-0.138, P=0.023) and urea levels (beta=0.146, P=0.036), and Gensini score (beta=0.317, P<0.001).
Conclusion: Findings of this study have shown that serum prolidase activity is significantly associated with the presence and severity of CAD, and elevated serum prolidase activity might be an independent predictor of coronary atherosclerosis.
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http://dx.doi.org/10.1097/MCA.0b013e32830042ba | DOI Listing |
J Obstet Gynaecol
December 2024
Department of Obstetrics and Gynecology, Health Sciences University, Etlik Zübeyde Hanım Women's Health Training and Research Hospital, Ankara, Turkey.
Prolidase is a manganese (Mn)-dependent cytosolic exopeptidase that degrades imidodipeptides with C-terminal proline or hydroxyproline. Prolidase recycling from imidodipeptides plays a critical role in collagen resynthesis and extracellular matrix (ECM) remodelling. Following an increase in gonadotropins, ovarian and follicular collagen undergo substantial degradation.
View Article and Find Full Text PDFUrologia
November 2024
Department of Chemistry, Yuzuncu Yil University, Van, Turkey.
Front Med (Lausanne)
April 2024
Department of Medical Biochemistry, Faculty of Medicine, Baskent University, Konya, Türkiye.
Objectives: Smoking causes inflammation, thickening, and narrowing of the airways. This inflammatory process is a reaction to free radicals and oxidants. Smoking affects collagen metabolism and tissue remodeling.
View Article and Find Full Text PDFUrol Oncol
April 2024
Department of Urology, Private Yuzyil Gebze Hospital, Kocaeli, Turkey. Electronic address:
Objectives: We aimed to identify serum prolidase activity, oxidative stress, and antioxidant enzyme levels in patients with prostate cancers and to evaluate their relationships with each other.
Materials And Methods: A total of 34 male patients with prostate cancer and with a mean age of 64.2 ± 4.
RMD Open
December 2023
Rheumatology and Immunology, Hannover Medical School, Hannover, Germany
Prolidase deficiency (PD) is a rare autosomal recessive inborn error of immunity caused by biallelic homozygous or compound heterozygous loss-of-function mutations in , the gene that encodes prolidase. PD typically manifests with variable dysmorphic features, chronic cutaneous ulcers, recurrent infections and autoimmune features, including systemic lupus erythematosus. So far, there is no consensus regarding treatment of PD and its autoimmune manifestations.
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