Eryptosis and oxidative damage in hypertensive and dyslipidemic patients

Carmen Elisa Pinzón-Díaz, José Víctor Calderón-Salinas, Margarita Marcela Rosas-Flores, Gerardo Hernández, Alicia López-Betancourt, Martha Angélica Quintanar-Escorza

Arterial hypertension is a disease that often coexists with dyslipidemia. Both disorders can produce oxidative stress. Studies in vivo and in vitro have proven that oxidative stress can induce an increment of the erythrocyte apoptosis (eryptosis), through the rise of free intracellular calcium concentration ([Ca(2+)]i). Higher levels of eryptosis have not been described in patients with hypertension, dyslipidemia, or both combined. This study involved 81 men between 26 and 50 years old, assorted into four groups: normotensive with and without dyslipidemia, and hypertensive with and without dyslipidemia. Hypertensive and/or dyslipidemic patients had double mean lipid peroxidation and 30% less mean GSH concentration than the normotensive non-dyslipidemic patients. Mean [Ca(2+)]i in hypertensive patients was 100 and 200% higher, in patients without and with dyslipidemia, respectively, compared to normotensive patients. Dyslipidemic normotensive patients had three times higher mean PS externalization than the normotensive non-dyslipidemic patients, and the hypertension condition doubled this difference. Hypertensive patients had higher eryptosis associated with higher levels of [Ca(2+)]i and oxidative stress, suggesting that eryptosis participates in the pathophysiological mechanisms of hypertension. The quantitative analysis, when the dyslipidemic factor is included, shows that oxidative stress-[Ca(2+)]i-eryptosis do not follow a unique pattern in the different groups and suggests the existence of mechanisms of induction and molecular pathways alternative or additional to oxidative stress and [Ca(2+)]i, respectively.