Polymorphism: an evaluation of the potential risk to the quality of drug products from the Farmácia Popular Rede Própria

Polymorphism in solids is a common phenomenon in drugs, which can lead to compromised quality due to changes in their physicochemical properties, particularly solubility, and, therefore, reduce bioavailability. Herein, a bibliographic survey was performed based on key issues and studies related to polymorphism in active pharmaceutical ingredient (APIs) present in medications from the Farmácia Popular Rede Própria. Polymorphism must be controlled to prevent possible ineffective therapy and/or improper dosage. Few mandatory tests for the identification and control of polymorphism in medications are currently available, which can result in serious public health concerns

Hydrogen sulfide cytoprotective signaling is endothelial nitric oxide synthase-nitric oxide dependent

Previous studies have demonstrated that hydrogen sulfide (H(2)S) protects against multiple cardiovascular disease states in a similar manner as nitric oxide (NO). H(2)S therapy also has been shown to augment NO bioavailability and signaling. The purpose of this study was to investigate the impact of H(2)S deficiency on endothelial NO synthase (eNOS) function, NO production, and ischemia/reperfusion (I/R) injury. We found that mice lacking the H(2)S-producing enzyme cystathionine γ-lyase (CSE) exhibit elevated oxidative stress, dysfunctional eNOS, diminished NO levels, and exacerbated myocardial and hepatic I/R injury. In CSE KO mice, acute H(2)S therapy restored eNOS function and NO bioavailability and attenuated I/R injury. In addition, we found that H(2)S therapy fails to protect against I/R in eNOS phosphomutant mice (S1179A). Our results suggest that H(2)S-mediated cytoprotective signaling in the setting of I/R injury is dependent in large part on eNOS activation and NO generation