Oxidative stress after sulfur mustard intoxication and its reduction by melatonin: efficacy of antioxidant therapy during serious intoxication
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Antioxidants administration & dosage therapeutic use MeSH
- Chemical Warfare Agents toxicity MeSH
- Injections, Intradermal MeSH
- Injections, Intraperitoneal MeSH
- Blood Proteins metabolism MeSH
- Rats MeSH
- Thiobarbituric Acid Reactive Substances metabolism MeSH
- Melatonin administration & dosage therapeutic use MeSH
- Poisoning blood metabolism prevention & control MeSH
- Oxidative Stress drug effects MeSH
- Rats, Wistar MeSH
- Mustard Gas toxicity MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Antioxidants MeSH
- Chemical Warfare Agents MeSH
- Blood Proteins MeSH
- Thiobarbituric Acid Reactive Substances MeSH
- Melatonin MeSH
- Mustard Gas MeSH
Sulfur mustard (SM) is an important chemical warfare agent. The mechanism of SM toxicity still has not been fully recognized. However, oxidative stress and following the damaging of macromolecules in the human body is considered one of the crucial steps in SM toxicity. Rats intoxicated with pure (i.e., distilled) SM were used as a model organism. The doses, 0 (control), 5, 20, and 80 mg/kg of body weight, were applied intradermally. A hormone with strong antioxidant potency, melatonin, was applied (25 and 50 mg/kg, subcutaneously) into the other group of rats exposed with the same doses of SM. Total plasma protein, ferric-reducing antioxidant power (FRAP), thiobarbituric-acid-reactive substances (TBARS), and plasma protein carbonyls were assayed in blood plasma. A significant decrease of total plasma proteins was found for control, and the lowest dose of SM was treated with melatonin. Melatonin was also able to enhance the production of low-molecular-weight antioxidants, as the SM-intoxicated rats had significantly (P ≤ 0.01) increasing FRAP levels after intoxication with SM in doses of 20 and 80 mg/kg, when compared to the control treated with melatonin. Melatonin also decreased TBARS level, representing reduced lipid peroxidation (LPO). However, LPO seems to be of less importance for SM toxic impact. The more reliable parameter was the level of total plasma protein carbonyls. The carbonyl levels were significantly increased due to SM, and the carbonylation was slowed due to melatonin intake. In conclusion, melatonin seems to be a prospective compound in reducing SM toxicity impact in the rat.
References provided by Crossref.org
Sulfur mustard induced oxidative stress and its alteration using asoxime (HI-6)