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Original Research

The Toxic Effects of Ethylene Glycol Tetraacetate Acid, Ferrum Lek and Methanol on the Glutathione System: correction Options

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Pages 131-139 | Received 01 Jun 2020, Accepted 10 Dec 2020, Published online: 23 Dec 2020
 

ABSTRACT

Objectives: The purpose of this study was to measure the level of lipid peroxidation and investigate the response of the glutathione system to toxic doses of ethylene glycol tetraacetate acid (EGTA), Ferrum Lek, methanol, and Depakine (valproate sodium).

Methods: This study focused on analyzing the toxic effects of EGTA, Ferrum Lek and methanol on lipid peroxidation processes and glutathione levels in animals. The study involved 375 outbred adult mice, of both sexes, weighing 28–31 g, and 100 outbred rats, weighing 180–200 g.

Results: After 14 days of valproate sodium/ademethionine treatment, the GR (glutathione reductase) activity in experimental animals continued to be higher than in controls. Using EGTA enhanced glutathione reductase and glutathione S transferase activities in the liver and kidney. The activity of glutathione peroxidase, however, increased only in the kidney (2.1-fold, p ≤ 0.001), while in the liver, a 31% drop was observed (p ≤ 0.05). The 15-mg and 30-mg doses of Ferrum Lek caused the liver level of thiobarbituric acid reactive substances to grow 3- and 3.5-fold, respectively (p ≤ 0.001).

Conclusion: The results of the study indicate that poisoning affected practically all components of the glutathione system. The oxidative stress was likely to result from an increased generation of reactive oxygen species against the background of inhibited antioxidant protection.

Article Highlights

  • EGTA enhances free radical processes in rat and mice tissues.

  • Decreased GP activity and decreased GSH together diminish the antioxidant defense system.

  • MDA after CPA is within the normal range, but GSH continues to be low.

  • L normalizes MDA, but causes GSH to grow.

  • Synergistic action of CPA+ L +EGTA reverts the GSH and enzyme activities to normal.

Disclosure statement

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Reviewer disclosures

Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.

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