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Titolo:
Hyperhomocyst(e)inemia induces multiorgan damage
Autore:
Miller, A; Mujumdar, V; Shek, E; Guillot, J; Angelo, M; Palmer, L; Tyagi, SC;
Indirizzi:
Univ Mississippi, Med Ctr, Sch Med, Dept Physiol & Biophys, Jackson, MS 39216 USA Univ Mississippi Jackson MS USA 39216 ol & Biophys, Jackson, MS 39216 USA
Titolo Testata:
HEART AND VESSELS
fascicolo: 3, volume: 15, anno: 2000,
pagine: 135 - 143
SICI:
0910-8327(2000)15:3<135:HIMD>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE MYOCARDIAL-INFARCTION; PRUNE-BELLY SYNDROME; CREATINE-KINASE MB; ATHEROSCLEROTIC LESIONS; HOMOCYSTEINE LEVELS; HYPERTENSIVE RATS; CORONARY-ARTERY; BLOOD-PRESSURE; HEART-FAILURE; NITRIC-OXIDE;
Keywords:
nerve; capillary endothelium; renal-ureter; hypertrophy; heart failure;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
43
Recensione:
Indirizzi per estratti:
Indirizzo: Tyagi, SC Univ Mississippi, Med Ctr, Sch Med, Dept Physiol & Biophys, 2500N State St, Jackson, MS 39216 USA Univ Mississippi 2500 N State St JacksonMS USA 39216 39216 USA
Citazione:
A. Miller et al., "Hyperhomocyst(e)inemia induces multiorgan damage", HEART VESS, 15(3), 2000, pp. 135-143

Abstract

Hyperhomocyst(e)inemia has been associated with the development of hypertension, stroke, and cardiovascular, cerebral/neuronal, renal, and liver diseases. To test the hypothesis that homocyst(e)ine plays an integrated role in multiorgan injury in hypertension, we employed: (1) spontaneously hypertensive rats (SHR) in which endogenous homocyst(e)ine levels are moderately high (18.1 +/- 0.5 muM); (2) control age- and sex-matched Wistar Kyoto (WKY)rats in which homocyst(e)ine levels are normal (3.7 +/- 0.3 CIM) To createthe pathophysiological condition of hyperhomocyst(e)inemia, 20mg/day homocyst(e)ine was administered for 12 weeks in (3) SHR (SHR-H) and in (4) WKY (WKY-H) rats, (5) Endogenous homocyst(e)ine levels were reduced slightly butnot significantly from 18.1 +/- 0.5 muM to 12.5 +/- 0.7 muM in SHR by folic acid administration (SHR-F), Plasma and tissue levels of homocyst(e)ine were determined by HPLC and spectrophotometric methods. Plasma and sympathetic ganglion (neuronal) matrix metalloproteinase (MMP) activity was measuredby zymography. Activity of neuronal MMP was increased in hyperhomocyst(e)inemic rats as compared with controls. Mean arterial pressure (mmHg) was 95 /- 5, 126 +/- 8,157 +/- 10, 188 +/- 5, and 165 +/- 12 in WKY, WKY-H, SHR, SHR-H, and SHR-F, respectively. Urinary protein (mg/day) was 0.11 +/- 0.03.0.88 +/- 0.22, 0.47 +/- 0.10, 0.89 +/- 0.21, and 0.81 +/- 0.21 in WKY, WKY-H, SHR, SHR-H, and SHR-F, respectively, as measured by the Bio-Rad dye binding assay. The relationships between increased arterial pressure, plasma homocyst(e)ine, and urinary protein were delineated. Plasma and neuronal creatinine phosphokinase (CK) isoenzymes were measured by agarose gel electrophoresis. All three CK isoenzymes, i.e., MM, MB, and BE, specific for skeletal, cardiac, and nerve tissue, respectively, were induced following 12 weeks hyperhomocyst(e)inemia. suggesting multiorgan injury by homocyst(e)ine. Homocyst(e)ine induces endocardial endothelial cell (capillary) apoptosis and may reduce capillary cell density. Structural damage to aorta, myocardium. kidney, and renal-ureter was analyzed by histology. Results suggested an integrated physiological role of homocyst(e)ine in injury to the endothelial/epithelial cell lining in the respective organs.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 22/09/20 alle ore 13:02:44