期刊
TOXICOLOGICAL SCIENCES
卷 122, 期 2, 页码 557-566出版社
OXFORD UNIV PRESS
DOI: 10.1093/toxsci/kfr143
关键词
citrinin; mouse skin; ROS; apoptosis; antioxidants
类别
资金
- Council of Scientific and Industrial Research (CSIR) [NWP-17]
- Council of Scientific and Industrial Research (CSIR), New Delhi [2940]
The mycotoxin, citrinin (CTN), is a contaminant of various food and feed materials. Several in vivo and in vitro studies have demonstrated that CTN has broad toxicity spectra; however, dermal toxicity is not known. In the present investigation, dermal exposure to CTN was undertaken to study oxidative stress, DNA damage, cell cycle arrest, and apoptosis in mouse skin. A single topical application of CTN caused significant change in oxidative stress markers, such as lipid peroxidation, protein carbonyl content, glutathione (GSH) content, and antioxidant enzymes in a dose-dependent (25-100 mu g/mouse) and time-dependent (12-72 h) manner. Single topical application of CTN (50 mu g/mouse) for 12-72 h caused significant enhancement in (1) reactive oxygen species (ROS); (2) cell cycle arrest at the G0/G1 phase (30-71%) and G2/M phase (56-65%) along with the induction of apoptosis (3.6-27%); (3) expression of p53, p21/waf1; (4) Bax/Bcl(2) ratio and cytochome c release; and (5) activities of caspase 9 (22-46%) and 3 (42-54%) as well as increased poly(ADP-ribose) polymerase cleavage. It was also observed that pretreatment with bio-antioxidants viz butylated hydroxyanisole (55 mu mol/100 mu l), quercetin (10 mu mol/100 mu l), or alpha-tocopherol (40 mu mol/100 mu l) resulted in decreases of ROS generation, arrest in the G0/G1 phase of the cell cycle, and apoptosis. These data confirm the involvement of ROS in apoptosis and suggest that these bio-antioxidants may be useful in the prevention of CTN-induced dermal toxicity.
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