Exposure to methyl tert-butyl ether (MTBE) is associated with mitochondrial dysfunction in rat

Abstract

1. Methyl tert-butyl ether (MTBE) is commonly used as an octane booster and oxygenate additive to gasoline. The assumed toxic effects of MTBE on human health are a matter of great debate. Exposure to MTBE has been shown to induce oxidative damage and no mechanistic explanation is available so far. Our goals were to determine whether MTBE is a mitochondrial toxicant, if so, what mechanism(s) is involved.

2. Male Sprague-Dawley rats were received MTBE in drinking water for 3 months. At the end of treatments, animals were killed, liver and blood samples were collected for biochemical and histopathological studies, and oxidative stress biomarkers. The rat liver mitochondria were isolated and several mitochondrial indices were measured.

3. We found that zinc plasma levels were remarkably declined with MTBE and N, N, N′, N′-Tetrakis (2-pyridylmethyl) ethylenediamine (TPEN; a zinc chelator) exposure. MTBE induced oxidative damage and caused mitochondrial dysfunctions in rats. Supplementation with zinc was able to protect against MTBE-induced cellular and sub-cellular toxicity.

4. Our results demonstrated that long-term exposure to MTBE is associated with zinc deficiency, oxidative stress, and mitochondrial energy failure in rat.

• Methyl tert-butyl ether (MTBE)
• mitochondrial dysfunction
• oxidative stress
• zinc deficiency

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Correction to: Exposure to methyl tert-butyl ether (MTBE) is associated with mitochondrial dysfunction in rat

Acknowledgements

We would like to thank Ayat Dashti and Omid Kohhi Hosseinabadi for performing the animal experiments and Asma Najibi for technical assistance. This work was supported by the Shiraz University of Medical Sciences grant for the accomplishment of the PhD thesis of Arastoo Saeedi (Grant number: 93-7312).

Declaration of interest

The authors declare no conflicts of interest.