Can exposure to cadmium and antimony promote oxidative stress and endothelial dysfunction?

Metal exposures are biologically credible contributors to oxidative and vascular injury. The evidence is strongest for cadmium; antimony has a similar experimental oxidative-stress profile but less direct human vascular evidence.

Oxidative-stress evidence

• Cadmium: Strong mechanistic evidence supports an indirect pro-oxidant effect. Cadmium binds cellular thiols, depletes glutathione, impairs antioxidant enzymes and mitochondrial electron transport—particularly complex I/III—thereby increasing reactive oxygen species (ROS), mitochondrial membrane-potential loss, and lipid, protein, and DNA oxidation. Occupational biomonitoring associations with oxidative-stress markers are directionally consistent, although smoking can modify observed associations.
• Antimony: Experimental evidence indicates interactions with cellular and mitochondrial thiols and inhibition of respiratory complexes. These effects can increase ROS, depolarize mitochondria, and trigger apoptotic signaling. Occupational observations linking urinary antimony with oxidative DNA damage are compatible with this pathway.

Endothelial and vascular effects

• Cadmium: Human findings support endothelial injury. In hemodialysis patients, serum cadmium was inversely associated with brachial flow-mediated dilation, a functional measure of endothelial nitric-oxide–dependent vasodilation. In adolescents and young adults, urinary cadmium showed dose-dependent associations with endothelial/platelet microparticles, markers of endothelial activation and apoptosis.
• Mechanistically, cadmium-driven NOX-derived superoxide, antioxidant depletion, and lipid peroxidation reduce nitric-oxide bioavailability and disrupt eNOS-related endothelial regulation. ROS also activates NF-κB, NLRP3, cytokines, and adhesion molecules, linking oxidative stress to vascular inflammation, permeability changes, and endothelial-cell death.
• Antimony: Endothelial-cell studies showing impaired angiogenesis and increased apoptosis make endothelial dysfunction biologically plausible, but direct human endothelial-function evidence has not been established.

Bottom line

• Cadmium can promote oxidative stress and is supported as a contributor to endothelial impairment. Antimony can promote oxidative stress and may impair endothelium through related mitochondrial, thiol, and apoptotic pathways, but its vascular effect remains less firmly demonstrated in humans.