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L‐2‐Oxothiazolidine‐4‐Carboxylic Acid Mitigates the Thromboembolic Effects and Systemic Toxicityinduced by Sub‐acute Exposure to Cadmiumin Mice
Author(s) -
Fahim Mohamed,
Nemmar Abderrahim,
Singh Sarabjit,
Shafiullah Mohamed,
Yasin Javed,
Hasan Mohamed
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.645.7
Subject(s) - superoxide dismutase , pharmacology , catalase , antioxidant , oxidative stress , toxicity , chemistry , cadmium , acute toxicity , medicine , biochemistry , organic chemistry
Exposure to cadmium (Cd) poses a deleterious health effects and its toxicity has been attributed to oxidative stress. Therefore, we examined the sub‐acute systemic and thrombotic influence of Cd exposure in vivo, and assessed the possible protective effects of the antioxidant L‐2‐Oxothiazolidine‐4‐Carboxylic acid (OTC). Mice received Cd at a dose of 1 mg Cd/kg/day, i.p., for 3 weeks. OTC pre‐treatment (80mg/kg/day, i.p.) was started one hour before Cd administration. Cd compared with control significantly reduced both the time (in seconds) for the first platelet aggregate (48.00 + 3.74 vs 79.33 + 20.73) and the time until blood flow stops (152 + 17.24 vs 179.00 + 13.62) in pial microvessels. OTC either by itself or concurrently with Cd significantly increased both the time for the first aggregate (156.67 + 10.98 vs 135.33 + 13.60) and until flow stops (239.00 + 20.22 vs 201.17 + 2.93). Cd induced a significant increase in total WBC and CK. A significant increase was also observed in liver enzymes after Cd exposure. The antioxidants Superoxide dismutase and catalase activities significantly increased in mice treated with Cd. OTC in combination with Cd alleviated most of these adverse effects induced by Cd. OTC, through its antioxidant actions, appeared to effectively protect Cd induced thrombosis in mice. Hence, OTC represents a potential candidate to protect the cerebral microvessels from the detrimental effect of Cd toxicity.