Aberrations in Oxidative Stress Markers in Amyotrophic Lateral Sclerosis: A Systematic Review and Meta-Analysis

الملخص EN

Oxidative stress has been reported to be involved in the onset and development of amyotrophic lateral sclerosis (ALS).

Data from clinical studies have highlighted increased peripheral blood oxidative stress markers in patients with ALS, but results are inconsistent.

Therefore, we quantitatively pooled data on levels of blood oxidative stress markers in ALS patients from the literature using a meta-analytic technique.

A systematic search was performed on PubMed and Web of Science, and we included studies analyzing blood oxidative stress marker levels in patients with ALS and normal controls.

We included 41 studies with 4,588 ALS patients and 6,344 control subjects, and 15 oxidative stress marker levels were subjected to random-effects meta-analysis.

The results demonstrated that malondialdehyde (Hedges’ g, 1.168; 95% CI, 0.812 to 1.523; P<0.001), 8-hydroxyguanosine (Hedges’ g, 2.194; 95% CI, 0.554 to 3.835; P=0.009), and Advanced Oxidation Protein Product (Hedges’ g, 0.555; 95% CI, 0.317 to 0.792; P<0.001) levels were significantly increased in patients with ALS when compared with control subjects.

Uric acid (Hedges’ g, -0.798; 95% CI, -1.117 to -0.479; P<0.001) and glutathione (Hedges’ g, -1.636; 95% CI, -3.020 to -0.252; P=0.02) levels were significantly reduced in ALS patients.

In contrast, blood Cu, superoxide dismutase, glutathione peroxidase, ceruloplasmin, triglycerides, total cholesterol, low-density lipoprotein, high-density lipoprotein, coenzyme-Q10, and transferrin levels were not significantly different between cases and controls.

Taken together, our results showed significantly increased blood levels of 8-hydroxyguanosine, malondialdehyde, and Advanced Oxidation Protein Product and decreased glutathione and uric acid levels in the peripheral blood of ALS patients.

This meta-analysis helps to clarify the oxidative stress marker profile in ALS patients, supporting the hypothesis that oxidative stress is a central component underpinning ALS pathogenesis.