Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2015 Jun 11:2:891-895.
doi: 10.1016/j.toxrep.2015.05.012. eCollection 2015.

A single acute hepatotoxic dose of CCl4 causes oxidative stress in the rat brain

Affiliations

A single acute hepatotoxic dose of CCl4 causes oxidative stress in the rat brain

K R Ritesh et al. Toxicol Rep. .

Abstract

Carbon tetrachloride (CCl4), a hepatotoxic agent is widely used to study the toxic mechanisms in experimental animals. We have investigated whether oxidative stress is induced in the brain at a single hepatotoxic dosage (1 ml/kg bw) of CCl4. Increased lipid peroxidation (LPO), protein carbonyls (PC) content and glutathione (GSH) depletion were observed in the brain regions of rats treated with CCl4 which was higher than that of liver. A drastic reduction in the activity of glutathione-S-transferase (GST) was seen in the brain regions which was higher than that of liver. Similarly, activities of glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT), NADH- and NADPH-dehydrogenase were reduced in the brain regions similar to that of liver. Higher induction of oxidative stress in the brain compared to that of liver implies vulnerability of the brain for CCl4 neurotoxicity. Our study shows that a single hepatotoxic dose of CCl4 is equally neurotoxic to rats.

Keywords: Antioxidant enzymes; Carbon tetrachloride; GSH; Neurotoxicity; Oxidative stress; ROS.

PubMed Disclaimer

Figures

Fig. 1
Fig. 1
CCl4-induced oxidative stress in the rat brain in comparison with the liver. LPO: Lipid peroxidation; PC: Protein carbonyls; GSH: Glutathione. Each bar represents the mean ± S.E, (n = 4). Data were analyzed by Independent Sample T test using SPSS version 14, (*˂ 0.05, ** ˂ 0.01, ***˂ 0.005). The numbers above the dark bar represent the percentage difference between control and treated groups.
Fig. 2
Fig. 2
CCl4-induced oxidative stress in the rat brain in comparison with the liver. GST: Glutathione-S-transferase; GPx: Glutathione peroxidase; GR: Glutathione reductase. Each bar represents the mean ± S.E, (n = 4). Data were analyzed by Independent Sample T test using SPSS version 14, (*˂ 0.05, ** ˂ 0.01, ***˂ 0.005). The numbers above the dark bar represent the percentage difference between control and treated groups.
Fig. 3
Fig. 3
CCl4-induced oxidative stress in the rat brain in comparison with the liver. SOD: Superoxide dismutase; CAT: Catalase; NADH-dehydrogenase; NADPH-dehydrogenase. Each bar represents the mean ± S.E, (n = 4). Data were analyzed by Independent Sample T test using SPSS version 14, (*˂ 0.05, ** ˂ 0.01, ***˂ 0.005). The numbers above the dark bar represent the percentage difference between control and treated groups.

References

    1. Halliwell B., Gutteridge J. Oxygen toxicity, oxygen radicals, transition metals and disease. Biochem. J. 1984;219(1):1–14. - PMC - PubMed
    1. Michael T.L., Beal M.F. Mitochondrial dysfunction and oxidative stress in neuro degenerative diseases. Nature. 2006;443:787–795. - PubMed
    1. Nathan C., Bussel A.C. Beyond oxidative stress on immunologists guide to reactive oxygen species. Nat. Rev. Immunol. 2013;13:349–361. - PMC - PubMed
    1. Forman H.J., Maiorino M., Ursini F. Signaling function of reactive oxygen species. Biochemistry. 2010;49:835–842. - PMC - PubMed
    1. Lokke H., Ragas M.J., Holmstrup M. Tools and perspectives for assessing chemical mixtures and multiple stressors. Toxicology. 2013;313:73–82. - PubMed

LinkOut - more resources