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Comparison of oxidative stress biomarkers in hypertensive patients with or without hyperhomocysteinemia
Gang Guo1, Wenjiang Sun2, Guanghui Liu3
1a Emergency Department , Tongji Hospital Affiliated to Tongji University , Shanghai , China.
Insights
Hyperhomocysteinemia exacerbates oxidative stress in hypertension, increasing cardiovascular risk. This study found higher oxidative stress markers and lower antioxidant levels in hypertensive patients with hyperhomocysteinemia compared to those without.
Area of Science:
- Cardiovascular Medicine
- Biochemistry
- Hypertension Research
Background:
- Hyperhomocysteinemia is a known risk factor for cardiovascular disease in hypertensive individuals.
- Oxidative stress plays a role in hypertension pathogenesis, but its specific impact in the presence of hyperhomocysteinemia is understudied.
Purpose of the Study:
- To compare oxidative stress biomarkers in hypertensive patients with and without hyperhomocysteinemia.
- To investigate the relationship between homocysteine levels and oxidative/antioxidative parameters in hypertension.
Main Methods:
- Compared serum levels of malondialdehyde (MDA), nitric oxide (NO), 8-isoprostane-F2ɑ, superoxide dismutase (SOD), catalase, and glutathione peroxides.
- Included 50 newly diagnosed hypertensive patients with hyperhomocysteinemia, 50 hypertensive patients without, and 50 healthy controls.
Main Results:
- Hypertensive patients, regardless of hyperhomocysteinemia, showed higher MDA and 8-isoprostane-F2ɑ and lower SOD and catalase than controls.
- Patients with hyperhomocysteinemia had significantly higher MDA and lower SOD levels than hypertensive patients without it.
- Homocysteine levels correlated positively with MDA and 8-isoprostane-F2ɑ and negatively with SOD and catalase.
Conclusions:
- Oxidative stress is more severe in hypertensive patients with hyperhomocysteinemia.
- Homocysteine may aggravate oxidative stress in hypertension, contributing to cardiovascular impairment.
Abstract:
Hyperhomocysteinemia is an independent risk factor for cardiovascular impairment in hypertension. Oxidative stress is important in the molecular mechanisms associated with hypertension, but there are few studies focusing on the comparison of oxidative stress biomarkers in hypertensive patients with or without hyperhomocysteinemia. The study included 50 newly diagnosed hypertensive patients with hyperhomocysteinemia, 50 newly diagnosed hypertensive patients without hyperhomocysteinemia, and 50 age-matched healthy controls. Serum levels of malondialdehyde, nitric oxide, 8-isoprostane-F2ɑ, superoxide dismutase, catalase, and glutathione peroxides were compared. Levels of malondialdehyde and 8-isoprostane-F2ɑ were higher in both hypertensive groups than in the control group (8.3 ± 1.8 μmol/L vs. 6.5 ± 1.3 μmol/L vs. 4.3 ± 1.2 μmol/L, P < 0.05; 23.5 ± 12.1 pg/mL vs. 17.4 ± 10.3 pg/mL vs. 13.9 ± 7.5 pg/mL, P < 0.05), while levels of superoxide dismutase and catalase were lower in both hypertensive groups than in the control group (120.5 ± 13.7 U/mL vs. 131.3 ± 18.2 U/mL vs. 149.1 ± 14.6 U/mL, P < 0.05; 23.8 ± 7.4 U/mL vs. 24.6 ± 9.2 U/mL vs. 33.5 ± 8.2 U/mL, P < 0.05). In hypertensive subgroups, serum malondialdehyde levels were higher in the hyperhomocysteinemia group than the other group (8.3 ± 1.8 μmol/L vs. 6.5 ± 1.3 μmol/L; P < 0.05), and superoxide dismutase activities were lower in the hyperhomocysteinemia group than the other group (120.5 ± 13.7 U/mL vs. 131.3 ± 18.2 U/mL; P < 0.05). Moreover, in hypertensive patients, homocysteine levels were significantly correlated with malondialdehyde (r = 0.39, P < 0.01), 8-isoprostane-F2ɑ (r = 0.47, P < 0.05), superoxide dismutase (r = -0.51, P < 0.01), and catalase (r = -0.51, P < 0.05), respectively. Our findings demonstrated oxidative stress was more severe in hypertensive patients with hyperhomocysteinemia than those hypertensive patients without it. Besides, there were strong relationships between homocysteine activities and oxidative/antioxidative parameters, which indicated that homocysteine might aggravate the oxidative stress in hypertension to produce contributory effects on cardiovascular impairment.
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