Plasma levels of total, free and protein bound thiols as well as sulfane sulfur in different age groups of rats.

Iciek, Małgorzata; Chwatko, Grażyna; Lorenc‐Koci, Elżbieta; Bald, Edward; Włodek, Lidia

doi:10.18388/abp.2004_3564

Cited by 74 publications

(31 citation statements)

References 38 publications

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“…A similar age-dependent decline in plasma tHcy levels was observed in apoE Ϫ/Ϫ mice fed methionine-enriched control or high-fat diets (36). Previous studies in rats (37) also showed that plasma levels of total, free, and protein-bound thiols, including homocysteine, decreased with age. These observations suggest that the age-dependent decline in plasma tHcy could be related to the induction of genes involved in intracellular homocysteine metabolism and/or export.…”

Section: Discussionsupporting

confidence: 68%

Hyperhomocysteinemia induced by methionine supplementation does not independently cause atherosclerosis in C57BL/6J mice

Zhou¹,

Werstuck²,

Lhoták³

et al. 2008

FASEB j.

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A causal relationship between diet-induced hyperhomocysteinemia (HHcy) and accelerated atherosclerosis has been established in apolipoprotein E-deficient (apoE −/− ) mice. However, it is not known whether the proatherogenic effect of HHcy in apoE −/− mice is independent of hyperlipidemia and/or deficiency of apoE. In this study, a comprehensive dietary approach using C57BL/6J mice was used to investigate whether HHcy is an independent risk factor for accelerated atherosclerosis or dependent on additional dietary factors that increase plasma lipids and/or inflammation. C57BL/ 6J mice at 4 wk of age were divided into 6 dietary groups: chow diet (C), chow diet + methionine (C+M), western-type diet (W), western-type diet + methionine (W+M), atherogenic diet (A), or atherogenic diet + methionine (A+M). After 2, 10, 20, or 40 wk on the diets, mice were sacrificed, and the levels of total plasma homocysteine, cysteine, and glutathione, as well as total plasma cholesterol and triglycerides were analyzed. Aortic root sections were examined for atherosclerotic lesions. HHcy was induced in all groups supplemented with methionine, compared to diet-matched control groups. Plasma total cholesterol was significantly increased in mice fed the W or A diet. However, the W diet increased LDL/IDL and HDL levels, while the A diet significantly elevated plasma VLDL and LDL/IDL levels without increasing HDL. No differences in plasma total cholesterol levels or lipid profiles were observed between methionine-supplemented groups and the diet-matched control groups. Early atherosclerotic lesions containing macrophage foam cells were only observed in mice fed the A or A + M diet. Furthermore, lesion size was significantly larger in the A + M group compared to the A group at 10 and 20 wk; however, mature lesions were never observed even after 40 wk on these diets. The presence of lymphocytes, increased hyaluronan staining, and the expression of endoplasmic reticulum (ER) stress markers were also increased in atherosclerotic lesions from the A + M group. Taken together, these results suggest that HHcy does not independently cause atherosclerosis in C57BL/6J mice even in the presence of increased total Clinical and epidemiological studies have established that elevated plasma total homocysteine (tHcy) is an independent risk factor for cardiovascular disease and stroke (1,2). Furthermore, accelerated atherosclerosis has been demonstrated in apolipoprotein E-deficient (apoE −/− ) mice with dietary hyperhomocysteinemia (HHcy) (3-5) and in cystathionine β-synthase (CBS)/apoE −/− double-knockout mice (6). These findings suggest that HHcy accelerates atherogenesis in a hyperlipidemic mouse model that develops spontaneous atherosclerosis. However, a causal relationship between atherogenesis and HHcy has not been established in other species, including rats, rabbits, pigs, and primates (7-10).Patients with inborn errors of methionine metabolism due to deficiencies in CBS or 5,10-methylenetetrahydrofolate reductase (MTHFR) present with severe...

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Section: Discussionsupporting

confidence: 68%

Hyperhomocysteinemia induced by methionine supplementation does not independently cause atherosclerosis in C57BL/6J mice

Zhou¹,

Werstuck²,

Lhoták³

et al. 2008

FASEB j.

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“…, 2008). Total sulfhydryl or thiol (T‐SH) content of the plasma is another parameter in evaluating the oxidative damage of proteins in plasma because 80% of plasma sulfhydryl content was reported to originate from plasma proteins (Iciek et al. , 2004; Candiano et al.…”

Section: Introductionmentioning

confidence: 99%

Plasma protein oxidation is correlated positively with plasma iron levels and negatively with hemolysate zinc levels in sickle‐cell anemia patients

Öztaş

Durukan

Ünal

et al. 2011

Int J Lab Hematology

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“…According to the literature, the levels of total plasma LMWT in rats are 75-200 µmol/l (Cys), 5-22 µmol/l (GSH) and 3.2-14.4 µmol/l (Hcy) [29][30][31]. It should be noted that age and diet (B 9 , fatty acid consumption) have a great impact on the total LMWT levels [30,32].…”

Section: Discussionmentioning

confidence: 99%

Plasma low-molecular-weight thiol/disulphide homeostasis as an early indicator of global and focal cerebral ischaemia

et al. 2017

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Plasma levels of total, free and protein bound thiols as well as sulfane sulfur in different age groups of rats.

Cited by 74 publications

References 38 publications

Hyperhomocysteinemia induced by methionine supplementation does not independently cause atherosclerosis in C57BL/6J mice

Hyperhomocysteinemia induced by methionine supplementation does not independently cause atherosclerosis in C57BL/6J mice

Plasma protein oxidation is correlated positively with plasma iron levels and negatively with hemolysate zinc levels in sickle‐cell anemia patients

Plasma low-molecular-weight thiol/disulphide homeostasis as an early indicator of global and focal cerebral ischaemia

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