Prototheca zopfii isolated from bovine mastitis induced oxidative stress and apoptosis in bovine mammary epithelial cells

// Muhammad Shahid 1 , Jian Gao 1 , Yanan Zhou 1 , Gang Liu 1 , Tariq Ali 1 , Youtian Deng 1 , Naveed Sabir 1 , Jingliang Su 1 , Bo Han 1 1 College of Veterinary Medicine, China Agricultural University, Beijing 100193, P R China Correspondence to: Bo Han, email: hanbo@cau.edu.cn Keywords: bovine mastitis, Prototheca zopfii, bMECs, apoptosis, oxidative stress Received: February 17, 2017      Accepted: March 19, 2017      Published: March 29, 2017 ABSTRACT Bovine protothecal mastitis results in considerable economic losses worldwide. However, Prototheca zopfii induced morphological alterations and oxidative stress in bovine mammary epithelial cells (bMECs) is not comprehensively studied yet. Therefore, the aim of this current study was to investigate the P. zopfii induced pathomorphological changes, oxidative stress and apoptosis in bMECs. Oxidative stress was assessed by evaluating catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), malondialdehyde (MDA) contents and lactate dehydrogenase (LDH) activity, while ROS generation and apoptosis was measured by confocal laser scanning microscopy. The results revealed that infection of P. zopfii genotype II (GTII) significantly changed bMECs morphology, increased apoptotic rate and MDA contents at 12 h ( p < 0.05) and 24 h ( p < 0.01) in comparison with control group, in time-dependent manner. LDH activity and ROS generation was also increased ( p < 0.01) at 12 h and 24 h. However, SOD and CAT contents in bMECs infected with GTII were decreased ( p < 0.05) at 12 h, while GPx ( p < 0.01), SOD ( p < 0.05) and CAT ( p < 0.01) levels were reduced at 24 h. In case of GTI, only CAT and GPx activities were significantly decreased when the duration prolonged to 24 h but lesser than GTII. This suggested that GTII has more devastating pathogenic effects in bMECs, and the findings of this study concluded that GTII induced apoptosis and oxidative stress in bMECs via the imbalance of oxidant and antioxidant defenses as well as the production of intracellular ROS.