Apoptosis and necroptosis in articular cartilage in rat induced by T-2 toxin under selenium deficient conditions
Zhang Ying, Jiang Zhuocheng, Fang Qian, Wang Wenjun, Zhang Meng, Wang Mengying, He Ying, Zhang Dan, Zhang Ying, Ma Tianyou, Chen Jinghong
Abstract
ObjectiveTo investigate the death of chondrocytes in rats which feed with T-2 toxin under selenium (Se) deficient conditions.
MethodsThirty two healthy male SD rats were divided into two groups by weight which were normal diet group and Se deficiency diet group, 16 rats in each group. Rats in normal diet group were fed with Se 101.5 μg/kg diet, and rats in Se deficiency diet group were fed with Se 1.1 μg/kg diet for 30 d. Normal diet group was divided into control group and T-2 toxin group, and Se deliciency diet group was randomly divided into Se-deficiency group and Se-deficiency plus T-2 toxin group, 8 rats in each group. After that, rats in T-2 toxin and Se-deficiency plus T-2 toxin groups were administrated intragastrically with T-2 toxin (100 μg/kg) everyday for 30 d. Rats were put to death, the left knee was taken and stained with hematoxylin-eosin and Safranin-Fast green, pathological changes of rat's knee joint cartilage were observed under light microscopy, expression levels of active caspase-3 and receptor interacting protein 3 (RIP3) in rat's articular cartilage cells were determined via the immunohistochemical method. The apoptosis was also detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL).
ResultsRed "ghost" outlines of chondrocyte and multiple chondral cell clusters surrounded the non-cell areas in deep zone of articular cartilage of knee joint stained with hematoxylin-eosin were seen in Se-deficiency plus T-2 toxin group under light microscope. In the superficial zone of cartilage, the positive percent of TUNEL and active caspase-3 in Se-deficiency plus T-2 toxin group was higher than those of control group, Se-deficiency group and T-2 toxin group [(7.47 ± 0.34)% vs (4.68 ± 0.54)%, (2.67 ± 0.64)%, (2.56 ± 0.54)%; (4.75 ± 0.67)% vs (1.24 ± 0.25)%, (0.00 ± 0.00)%, (0.00 ± 0.00)%, P < 0.05]. In the middle zone of cartilage, the positive percent of TUNEL, active caspase-3 and RIP3 in Se-deficiency plus T-2 toxin group was significantly higher than those of control group, T-2 toxin group and Se-deficiency group [(72.06 ± 6.15)% vs (16.10 ± 3.00)%, (19.57 ± 3.49)%, (19.33 ± 5.19)%; (51.13 ± 4.18)% vs (10.97 ± 3.01)%, (15.36 ± 4.37)%, (15.23 ± 3.13)%; (25.91 ± 13.39)% vs (1.59 ± 1.14)%, (4.32 ± 2.91)%, (7.50 ± 5.00)%, P < 0.05]. The positive percents of TUNEL, active caspase-3 and RIP3 were not significantly different in the deep zone ( P > 0.05).
ConclusionThe death of the middle zone in the rat cartilage induced by T-2 toxin under selenium deficient conditions is apoptosis and necroptosis.
Key words:
Kashin-Beck disease; Apoptosis; Necrosis; T-2 toxin; Selenium
Contributor Information
Zhang Ying
National Health and Family Planning Commission Key Laboratory of Environment and Genes Related to Diseases, Institute of Endemic Diseases, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an 710061, China
Jiang Zhuocheng
National Health and Family Planning Commission Key Laboratory of Environment and Genes Related to Diseases, Institute of Endemic Diseases, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an 710061, China
Fang Qian
National Health and Family Planning Commission Key Laboratory of Environment and Genes Related to Diseases, Institute of Endemic Diseases, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an 710061, China
Wang Wenjun
National Health and Family Planning Commission Key Laboratory of Environment and Genes Related to Diseases, Institute of Endemic Diseases, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an 710061, China
Zhang Meng
National Health and Family Planning Commission Key Laboratory of Environment and Genes Related to Diseases, Institute of Endemic Diseases, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an 710061, China
Wang Mengying
National Health and Family Planning Commission Key Laboratory of Environment and Genes Related to Diseases, Institute of Endemic Diseases, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an 710061, China
He Ying
National Health and Family Planning Commission Key Laboratory of Environment and Genes Related to Diseases, Institute of Endemic Diseases, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an 710061, China
Zhang Dan
National Health and Family Planning Commission Key Laboratory of Environment and Genes Related to Diseases, Institute of Endemic Diseases, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an 710061, China
Zhang Ying
National Health and Family Planning Commission Key Laboratory of Environment and Genes Related to Diseases, Institute of Endemic Diseases, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an 710061, China
Ma Tianyou
National Health and Family Planning Commission Key Laboratory of Environment and Genes Related to Diseases, Institute of Endemic Diseases, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an 710061, China
Chen Jinghong
National Health and Family Planning Commission Key Laboratory of Environment and Genes Related to Diseases, Institute of Endemic Diseases, School of Public Health, Health Science Center, Xi'an Jiaotong University, Xi'an 710061, China