Obesity is an important preventable risk factor for morbidity and mortality from cardiometabolic disease. Oxidative stress (including in visceral adipose tissue) and chronic low-grade
inflammation are the major underlying pathomechanisms.
Monoamine oxidase (
MAO) has recently emerged as an important source of cardiovascular oxidative stress. The present study was conducted to evaluate the role of
MAO as contributor to
reactive oxygen species (ROS) production in white adipose tissue and vessels harvested from patients undergoing elective abdominal surgery. To this aim, visceral adipose tissue and mesenteric artery branches were isolated from obese patients with chronic
inflammation and used for organ bath, ROS production, quantitative real-time PCR, and immunohistology studies. The human visceral adipose tissue and mesenteric artery branches contain mainly the
MAO-A isoform, as shown by the quantitative real-time PCR and immunohistology experiments. A significant upregulation of
MAO-A, the impairment in vascular reactivity, and increase in ROS production were found in obese vs. non-obese patients. Incubation of the adipose tissue samples and
vascular rings with the
MAO-A inhibitor (
clorgyline, 30 min) improved vascular reactivity and decreased ROS generation. In conclusion,
MAO-A is the predominant
isoform in human abdominal adipose and vascular tissues, is overexpressed in the setting of
inflammation, and contributes to the endothelial dysfunction.