α-Lipoic acid is a potent antioxidant, and also an essential cofactor for PDH and α-KDH complexes in mitochondria. Investigations have shown complex human diseases are associated with oxidative stress. As preventative and therapeutic purposes, studies have evaluated effects of lipoic acid on complex human diseases, however, its molecular mechanisms and effects remained unknown. In this study, we examined the effects of heterozygous Lias deficiency on LPS induced inflammation and adrenergic agonist induced cardiac hypertrophy. We observed increased sensitivity of Lias heterozygous mice with elevation of TNF-α, decreased and delayed recovery of leukocyte and platelet counts accompanied with liver necrosis lung inflammation on LPS stimuli. Upon adrenergic agonist stimulation, both genotypes developed hypertrophy with increased HW/BW ratio and fibrosis in the heart, however, we observed protective effect of Lias deficiency upon stimulation. Our data indicates that Lias deficiency results in increased sensitivity upon LPS stimulation, however, protective effect against cardiac stimulation
