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Background: Leptin is an adipokine encoded by the Ob (obese) gene and predominantly produced by adipocytes. The roles of both leptin and leptin receptor (ObR) in numerous pathophysiological conditions including mammary tumor (MT) development have been reported. Aim: To examine protein expression levels of leptin and its receptors (ObR) including the long form, ObRb, in MT tissue and mammary fat pad of a transgenic mammary cancer mouse model. Further, we investigated whether the effects of leptin on MT development are systemic or local. Materials and Methods: MMTV-TGF-α transgenic female mice were fed ad libitum from week 10 up to week 74. Protein expression levels of leptin, ObR, and ObRb were measured in the mammary tissue samples of 74-week old MMTV-TGF-α mice with and without MT (MT-positive/MT-negative) by Western blot analysis. Serum leptin levels were measured by using the mouse adipokine LINCOplex kit 96-well plate assay. Results: Protein expression levels of ObRb were significantly lower in MT as compared to control tissue of mammary gland. In addition, protein expression levels of leptin were significantly higher in the MT tissue of MT-positive mice compared to control tissue of MT-negative mice. However, ObR protein expression levels in tissues of mice with and without MT were similar. Serum leptin levels at different ages were not significantly different between the two groups. Conclusion: Leptin and ObRb in the mammary tissue may play a critical role in the mammary cancer development, while contribution of short ObR isoform may be less important.

Hypochlorous acid (HOCl) is a strong oxidant produced by activated neutrophils via the myeloperoxidase (MPO) enzyme in order to fight against infections. Because of their antimicrobial and antiviral properties, stabilized HOCl solutions were produced to be used as a disinfectant and became a recommended disinfectant against COVID-19 by the US Environmental Protection Agency. Aberrant MPO enzyme activity results in abundant HOCl production which is related to the development and/or progression of several diseases including atherosclerosis, cardiovascular and neurodegenerative diseases. Previous studies investigating the effect of HOCl on the mode of cell death in different cell types reported that HOCl induces both apoptosis and necrosis depending on its concentration. However, the data on the apoptotic pathway triggered by HOCl is controversial. In this study, we investigated the mode of cell death induced by different concentrations of HOCl in Saccharomyces cerevisiae. Our data revealed that HOCl leads to cell death within 1 minute at 170 µM and above. At 340 µM, HOCl causes a rapid necrosis, while 170 µM HOCl leads to apoptosis. HOCl-induced apoptosis is mostly caspase dependent and Aif1 doesn't have a significant role.