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Weill-Marchesani syndrome (WMS) is a rare systemic disorder with both autosomal recessive and dominant inheritances. Accumulation of reactive oxygen species such as O2*-, H2O2 and OH* causes lipid peroxidation (LPO), whereas antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GSHPx)) mediate defence against oxidative stress. Excess tumour necrosis factor (TNF)-alpha and NO* react with O2*- and cause further antioxidant depletion with an increase in mutation frequency by H2O2. This study investigated the levels of SOD, GSHPx, catalase (CAT), TNF-alpha, NO and LPO in patients with WMS.

mediators of inflammation

Tumour necrosis factor α, lipid peroxidation and NO are increased and associated with decreased free-radical scavenging enzymes in patients with Weill-Marchesani syndrome

Tumour necrosis factor α, lipid peroxidation and NO are increased and associated with decreased free-radical scavenging enzymes in patients with Weill-Marchesani syndrome

Tumour necrosis factor α, lipid peroxidation and NO are increased and associated with decreased free-radical scavenging enzymes in patients with Weill-Marchesani syndrome