Bacteriophage therapy: back to the future

In connection with growing problem of antimicrobial resistance, the search for alternative treatments for infection is popular topic nowadays. This article represents an overview of published data on the therapeutic use of bacteriophages, specifically in urinary tract infections. The history of phage therapy of infectious diseases from the beginning of the 20th century to the present days is presented. The paper also discuss the mechanism of bacteriophages activity, differences between lytic and lysogenic phages, mechanisms of bacterial tolerance to phages and ways of its overcoming are. Authors present their own data on 30 years of clinical use of “bacteriophage cocktails” in the treatment and prevention of urological infection

The role of mitochondria in oxidative and nitrosative stress during ischemia/reperfusion in the rat kidney

Reoxygenation following ischemia causes tissue oxidative stress. We studied the role of oxidative stress caused by kidney ischemia/reperfusion (I/R) on the mitochondria of renal tissue slices. I/R caused the mitochondria to be swollen, fragmented, and have lower membrane potential. The mitochondria generated more reactive oxygen species (ROS) and nitric oxide (NO) in situ as measu red by fluorescence of ROS- and NO-sensitive probes. Infusion of lithium ion, an inhibitor of glycogen kinase synthase-3, caused phosphorylation of its Ser-9 and restored the membrane potential and decreased ROS production of the mitochondrial fraction. Ischemic kidney and hypoxic rat preconditioning improved mitochondrial membrane potential and lowered ROS production caused by subsequent I/R similar to lithium ion infusion. Preconditioning normalized NO production in mitochondria as well. The drop in the mitochondrial membrane potential was prevented by NO synthase inhibition, demonstrating a strong contribution of NO to changes in mitochondrial energy metabolism during the I/R transition. Mitochondria in the I/R-stressed kidney contained less cytochrome c and more pro-apoptotic Bax, consistent with apoptotic degradation