Redox Status in Patients Suffering from Multiple Chemical Sensitivity (MCS): A Pilot Study
Metadatos
Mostrar el registro completo del ítemAutor
Aranda Martínez, Paula; Menéndez-Coto, Nerea; Coto-Montes, Ana; Martín-Estebané, María; Escames Rosa, Germaine; Acuña-Castroviejo, DaríoEditorial
MDPI
Materia
Multiple chemical sensitivity Oxidative stress Glutathione
Fecha
2025-09-02Referencia bibliográfica
Aranda-Martínez, P.; Menéndez-Coto, N.; Coto-Montes, A.; Martín-Estebané, M.; Escames, G.; Acuña-Castroviejo, D. Redox Status in Patients Suffering from Multiple Chemical Sensitivity (MCS): A Pilot Study. J. Clin. Med. 2025, 14, 6185. https://doi.org/10.3390/jcm14176185
Patrocinador
ASESSCA association (Asturias, Spain)Resumen
Background/Objectives: Multiple chemical sensitivity (MCS) is a complex environmental
illness characterized by intolerance to various environmental chemicals, affecting multiple
organ systems. Despite its prevalence, MCS remains poorly understood, with limited
recognition by the World Health Organisation amid challenges in diagnosis due to symptom heterogeneity. This study aimed to investigate the oxidative stress status in patients
diagnosed with MCS compared to healthy controls, focusing on plasma and erythrocyte
markers. Methods: Blood samples from 40 MCS patients and 40 controls were analyzed
for lipid peroxidation (LPO), total antioxidant activity (TAA), adenosine triphosphate
(ATP), and antioxidant enzyme activities, alongside glutathione cycle components. Results:
Results revealed no significant differences in plasma LPO or TAA between groups, with
a reduction in 61% ATP levels in MCS subjects. However, erythrocyte analysis showed
reduced levels of glutathione (GSH) and total glutathione in MCS patients. Glutathione
peroxidase (GPx) activity also decreased by 15% in erythrocytes of MCS patients, suggesting increased hydrogen peroxide detoxification at the expense of oxidation of GSH
to glutathione disulfide (GSSG). Because glutathione reductase activity (GRd) did not
change, this GSSG could not be reduced, the GSSG/GSH ratio increased by 46%, indicating
heightened intracellular oxidative stress. Catalase (CAT) activity also remained unchanged
(reduced by 9%, non-significant). Conclusions: These findings highlight the role of oxidative stress in MCS pathophysiology, particularly the disruption of the glutathione cycle
within erythrocytes. The study underscores the need for further research into the molecular
mechanisms underlying MCS to improve diagnostic criteria and therapeutic strategies.
Understanding intracellular oxidative imbalances may provide insights into the systemic
dysfunction observed in MCS patients.





