Alterations in antioxidant function and cell apoptosis in spleens of duck exposed to molybdenum or/and cadmium
Mengmeng Zhang, Junrong Luo, Caiying Zhang*, Huabin Cao*, Bing Xia, Guoliang Hu
Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agriculture University, Jiangxi, China
Correspondence to: Tel: +86-791-83813503; Fax: +86-791-83813504;
E-mail: zhangcaiying0916@163.com (C Zhang), chbin20020804@163.com (H Cao)
The first two authors contributed equally to this work.
Received: October 14, 2015; Revised: March 23, 2016; Accepted: May 12, 2016; Published online: June 13, 2016.
Abstract
The present study is designed to research the effects of molybdenum (Mo) or/and cadmium (Cd) on antioxidant function and the apoptosis-related genes in duck spleens. Sixty healthy eleven-day-old ducks were randomly divided into to six groups with equal number (control group, LMo group, HMo group, Cd group, LMo+Cd group, HMo+Cd group) which were fed with basal diet containing variable doses of Mo or/and Cd. Relative weight of spleen, antioxidant indexes, apoptosis-related genes mRNA expression levels and ultrastructural changes were evaluated on 120 days. The results showed that relative weight of spleen was decreased in treatment groups. Malondialdehyde (MDA) level was increased, while the activities of xanthine oxidase (XOD) and catalase (CAT) were decreased in Mo or/and Cd groups compared with control group. Bak-1 and Caspase-3 expressions were up-regulated in high dose of Mo combined with Cd group, while Bcl-2 was down-regulated. What’s more, mitochondrial crest fracture, swelling, vacuolation, deformed nuclei and karyopyknosis in Mo+Cd combination treated groups were more severe. The results suggested that Mo or/and Cd could induce oxidative stress, apoptosis of spleen associated with mitochondrial intrinsic pathway, and the two elements show possible synergistic relationship.
Keywords: apoptosis, cadmium, duck, molybdenum, oxidative stress


© 2016 The Korean Society of Veterinary Science.