Forskolin attenuates doxorubicin-induced accumulation of asymmetric dimethylarginine and s-adenosylhomocysteine via methyltransferase activity in leukemic monocytes.

Doxorubicin (DOX) is an antitumor drug, associated with cardiomyopathy. Strategies to address DOX-cardiomyopathy are scarce. Here, we identify the effect of forskolin (FSK) on DOX-induced-asymmetric-dimethylarginine (ADMA) accumulation in monocytoid cells. DOX-challenge led to i) augmented cytotoxicity, reactive-oxygen-species (ROS) production and methyltransferase-enzyme-activity identified as ADMA and s-adenosylhomocysteine (SAH) accumulation (SAH-A). However, except cytotoxicity, other DOX effects were decreased by metformin and FSK. FSK, did not alter the DOX-induced cytotoxic effect, but, decreased SAH-A by >50% and a combination of three drugs restored physiological methyltransferase-enzyme-activity. Together, protective effect of FSK against DOX-induced SAH-A is associated with mitigated methyltransferase-activity, a one-of-a-kind report.

Polycystic ovarian syndrome-associated cardiovascular complications: An overview of the association between the biochemical markers and potential strategies for their prevention and elimination.

Polycystic ovarian syndrome (PCOS) is associated with multiple cardiovascular risk factors (CVRF) including endothelial dysfunction (ED) and presence of metabolic syndrome (MS). The probable reason suggested for elevated CVRF in PCOS is oxidative stress (OS), which is an integral factor in cardiometabolic complications (CMC) seen in PCOS women. The interrelated mechanisms by which CVRF instigate clinical manifestation plays a crucial role in identification of a strategy to treat different comorbidities in PCOS. The existing treatment for PCOS mostly focuses on management of individual disorders, however, therapeutic strategies or novel targets to address cardiovascular complications in PCOS deserve extensive analysis.