Homocysteinemia, hypertension, and family history of diabetes in a smoking male population in Saudi Arabia

Al-Daghri, Nasser M.; Al‐Attas, Omar S.

doi:10.2478/s11536-008-0019-9

Cited by 1 publication

(2 citation statements)

References 33 publications

(32 reference statements)

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“…In the last period, evidence concerning homocysteine involvement in thrombosis and cardiovascular diseases has been accumulated [1][2][3][4][5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

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Hyperhomocysteinemia’s effect on antioxidant capacity in rats

et al. 2010

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AbstractHyperhomocysteinemia represents elevated homocysteine (Hcys) concentrations in blood above the normal range. In humans, the normal range of homocysteine is 5.0–15.9 mM/ml. High levels of homocysteine disturb the normal epithelial functions and correlate with cardiovascular diseases even at slightly increased concentrations. In homocysteine metabolism, vitamins play an important role. The mechanism through which homocysteine triggers these effects is not yet elucidated, but the involvement of reactive species may be the answer. It is not known whether the intra- or extracellular antioxidant system is more affected by elevated homocysteine levels. We studied the effects of hyperhomocysteinemia on the intra- and extracellular antioxidant defense systems in two different types of diet in rats. Type I was food with low folic acid and vitamin B12 content and type II was food with normal amounts of these two vitamins. Hyperhomocysteinemia was experimentally induced by oral administration of methionine 2 mg/kg body weight, single daily dose, for a 15-day period. Plasma concentrations of homocysteine were measured using an HPLC method. In the response of the intracellular antioxidant defense system against hyperhomocysteinemia, we determined the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in red blood cells, using RANDOX kits for manual use. For the extracellular response we determined the plasma total antioxidant status (TAS) also using a RANDOX kit for manual use. Our data show that methionine load induces hyperhomocysteinemia despite normal vitamin supply in rats. SOD activity rose with simultaneous decrease in GPx activity independently of diet; this might suggest that the intracellular defense system was disturbed by the rise in homocysteine level. TAS decrease suggests that the extracellular antioxidant defense was also affected. We assume that hyperhomocysteinemia is directly linked to reactive species generation and the intracellular space seems to be more affected than the extracellular one.

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“…In the last period, evidence concerning homocysteine involvement in thrombosis and cardiovascular diseases has been accumulated [1][2][3][4][5][6][7][8][9].…”

Section: Introductionmentioning

confidence: 99%

“…Some genetic polymorphisms of methyltetrahydrofolate reductase and cystathionine synthetase, as well as inappropriate supplies of folic acid (B 9 ), pyridoxine (B 6 ), or cyanocobalamine (B 12 ), cause a decrease in methionine metabolism and, as a consequence, an increase in homocysteine blood concentration [10][11][12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%