Abstract
BackgroundExposures to environmental toxins are now thought to contribute to the development of autism spectrum disorder. Propionic acid (PA) found as a metabolic product of gut bacteria has been reported to mimic/mediate the neurotoxic effects of autism. Results from animal studies may guide investigations on human populations toward identifying environmental contaminants that produce or drugs that protect from neurotoxicity. Forty-eight young male Western Albino rats were used in the present study. They were grouped into six equal groups 8 rats each. The first group received a neurotoxic dose of buffered PA (250 mg/Kg body weight/day for 3 consecutive days). The second group received only phosphate buffered saline (control group). The third and fourth groups were intoxicated with PA as described above followed by treatment with either coenzyme Q (4.5 mg/kg body weight) or melatonin (10 mg/kg body weight) for one week (therapeutically treated groups). The fifth and sixth groups were administered both compounds for one week prior to PA (protected groups). Heat shock protein70 (Hsp70), Gamma amino-butyric acid (GABA), serotonin, dopamine, oxytocin and interferon γ-inducible protein 16 together with Comet DNA assay were measured in brain tissues of the six studied groups.ResultsThe obtained data showed that PA caused multiple signs of brain toxicity revealed in depletion of GABA, serotonin, and dopamine, are which important neurotransmitters that reflect brain function, interferon γ-inducible protein 16 and oxytocin. A high significant increase in tail length, tail DNA% damage and tail moment was reported indicating the genotoxic effect of PA. Administration of melatonin or coenzyme Q showed both protective and therapeutic effects on PA–treated rats demonstrated in a remarkable amelioration of most of the measured parameters.ConclusionIn conclusion, melatonin and coenzyme Q have potential protective and restorative effects against PA-induced brain injury, confirmed by improvement in biochemical markers and DNA double strand breaks.
Highlights
Exposures to environmental toxins are thought to contribute to the development of autism spectrum disorder
After one week of acclimation, the rats were divided into six groups, namely the control group in which animals were fed normal diet during the experimental period; the Propionic acid (PA) treated rats that received 250 mg/kg body weight/day for 3 days, in order to induce autistic features; The third and fourth groups were treated with low dose of either coenzyme Q (4.5 mg/kg body weight) [29] or melatonin (10 mg/kg body weight) [30] for one week after being intoxicated with the PA as described above
It was noticed that PA induced remarkable decrease in all parameters
Summary
Exposures to environmental toxins are thought to contribute to the development of autism spectrum disorder. Propionic acid (PA) found as a metabolic product of gut bacteria has been reported to mimic/ mediate the neurotoxic effects of autism. Results from animal studies may guide investigations on human populations toward identifying environmental contaminants that produce or drugs that protect from neurotoxicity. Forty-eight young male Western Albino rats were used in the present study. They were grouped into six equal groups 8 rats each. The first group received a neurotoxic dose of buffered PA (250 mg/Kg body weight/day for 3 consecutive days). PA is produced by fermentation of polysaccharides, oligosaccharides, long-chain fatty acids, protein, peptides and glycoprotein precursors by the anaerobic colonic microbiota, Undigested carbohydrates, such as dietary fibers and resistant starch, represent the major source for PA production [3]. PA is a short chain fatty acid formed endogenously in the human body as an intermediate of fatty acid metabolism and a metabolic end product of enteric gut microbiota such as clostridia and propionibacteria [3]
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