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Published on: June 14, 2016
Dynamic thiol/disulphide homeostasis in patients with hypertrophic cardiomyopathy
Munevver Sari1, Unal Erkorkmaz2, Hayrullah Yazar3
1Department of Cardiology, University of Health Sciences, Kartal Kosuyolu Education and Research Hospital, Denizer street, 34865, Kartal/Istanbul, Turkey. benmsr@hotmail.com.
Insights
Patients with hypertrophic cardiomyopathy (HCM) exhibit altered serum thiol/disulphide homeostasis, indicating impaired antioxidant capacity. This suggests a potential link between HCM and oxidative stress similar to that observed in tumors.
Area of Science:
- Biochemistry
- Cardiology
- Oxidative Stress Research
Background:
- Hypertrophic cardiomyopathy (HCM) presents complex genetic factors and variable clinical outcomes.
- Investigating non-genetic factors like oxidative stress is crucial for understanding HCM's heterogeneity.
Purpose of the Study:
- To evaluate serum thiol/disulphide homeostasis as a marker of oxidative stress in patients with HCM.
- To utilize a novel automated assay for precise measurement of thiol/disulphide balance.
Main Methods:
- A cross-sectional study involving 119 HCM patients and 52 controls.
- Measurement of dynamic thiol/disulphide homeostasis using calorimetric and duplex methods developed in 2014.
Main Results:
- HCM patients showed significantly lower serum native thiol, total thiol, and disulphide levels compared to controls.
- Disulphide/native thiol and disulphide/total thiol ratios were significantly lower in HCM patients.
- Reduced thiol ratios were higher, and oxidized thiol ratios were lower in HCM patients, indicating impaired antioxidant capacity.
Conclusions:
- HCM patients exhibit impaired antioxidant capacity, with serum thiol/disulphide homeostasis shifted towards a reducing state.
- The study speculates that HCM may share similarities with tumors regarding serum thiol-disulphide level alterations.
Background:
In addition to the genetic complexity of hypertrophic cardiomyopathy (HCM), there must be other disease-modifying factors that contribute to its highly variable clinical and phenotypic expression. The authors aimed to investigate serum thiol/disulphide homeostasis as a proxy for oxidative stress using a novel automated assay in patients with HCM.
Methods:
This cross-sectional study was conducted on 119 patients with HCM and 52 without HCM. The methods used to measure dynamic thiol/disulphide homeostasis as calorimetric and duplex quantities were developed in 2014.
Results:
Median serum native thiol levels were significantly lower in patients with HCM than in those without (312.5 μmol/L [285-370 μmol/L] vs 421 μmol/L [349-469.5 μmol/L]; p < 0.001). Serum total thiol levels and disulphide levels were considerably lower than those in the control group ([844.68 ± 195.99 μmol/L vs 1158.92 ± 243.97 μmol/L; p < 0.001], [259.13 ± 65.66 μmol/L vs 375.02 ± 79.99 μmol/L; p < 0.001], respectively). Serum disulphide/native thiol ratios and disulphide/total thiol ratios were significantly lower in HCM patients than in controls (0.80 ± 0.09 vs 0.92 ± 0.05; p < 0.001 and 0.31 [0.30-0.32] vs 0.32 [0.32-0.33]; p < 0.001). Finally, reduced thiol ratios were higher and oxidized thiol ratios were significantly lower in patients with HCM than in controls.
Conclusions:
Despite the fact that antioxidant capacity was impaired, the extracellular environment remained in a reducing state by keeping serum disulphide/native thiol ratios low. Therefore, the authors speculate that HCM may behave similarly to tumours with respect to serum thiol-disulphide levels.
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