Assessing Mitochondrial Function, Oxidative Stress and Vitamin D Status in Dark-Skinned Patients With Keloid Disease

Keloid disease, marked by excessive fibrous tissue growth, is prevalent in dark-skinned individuals. Mitochondrial integrity is essential for wound healing through cytoskeletal remodelling. Altered mitochondrial morphology and reactive oxygen species (ROS) signalling may underlie keloid pathology, which may be worsened by vitamin D insufficiency.

To investigate vitamin D status, mitochondrial function and oxidative stress in keloid disease.

Keloid tissue and whole blood were collected from 44 dark-skinned patients (18-65 years). Plasma vitamin D levels were quantified by routine analysis. Plasma malondialdehyde (MDA), a lipid peroxidation marker, was measured using the thiobarbituric acid reactive substance assay. Mitochondrial DNA (mtDNA) integrity was assessed by quantitative PCR in keloid tissue, and mitochondrial morphology was examined with transmission electron microscopy (TEM).

Among the 44 patients, 30 had normal vitamin D levels, 13 had low levels and 1 was deficient. Oxidative stress marker, MDA and mtDNA integrity were similar across vitamin D groups. No association was observed between vitamin D and plasma MDA levels. An inverse relationship emerged between mtDNA integrity and plasma MDA (r = -0.5225, CI -0.751--0.0182, p = 0.0036), while vitamin D positively correlated with mtDNA integrity (r = 0.402, CI 0.052-0.665, p = 0.0224). TEM revealed subtle mitochondrial alterations in patients with low vitamin D, including reduced size, and double-membrane outlines were visible in several micrographs, whereas others showed less pronounced boundary contrast.

Vitamin D insufficiency was uncommon in this cohort. While oxidative stress marker, MDA and mtDNA integrity did not differ by vitamin D status, structural mitochondrial changes were observed in dark-skinned keloid patients with low vitamin D.