Abstract
BackgroundPropionic acid (PA) found in some foods and formed as a metabolic product of gut bacteria has been reported to mimic/mediate the effects of autism. The present study was undertaken to compare the effect of orally administered PA with that of clindamycin-induced PA-microbial producers in inducing persistent biochemical autistic features in hamsters. The neuroprotective potency of carnosine and carnitine supplements against PA toxicity was also investigated.MethodsThe following groups were studied. 1. Control group, which received phosphate buffered saline orally, 2. Propionic acid treated group which were given PA at a dose of 250 mg/kg body weight/day for 3 days orally, 3. Clindamycin treated group which received a single dose of the antibiotic orogastrically at a dose of 30 mg/kg on the day of the experiment, 4. Carnosine-treated group which were given carnosine at a dose of 10 mg/kg body weight/day orally for one week, 5. Carnitine treated group given 50 mg/kg body weight/day carnitine orally daily for one week. Group 6. Carnosine followed by PA, Group 7. Carnitine followed by PA. Dopamine, adrenaline and noradrenaline, serotonin and Gamma amino-butyric acid (GABA) were measured in the cortex and medulla of the nine studied groups.ResultsPA administration caused significant decrease in the neurotransmitters in the brains of treated hamsters while clindamycin caused a significant decrease only in dopamine in hamster brains (cortex and medulla) and GABA in the cerebral cortex of the treated hamsters. Administration of carnosine and carnitine which are known antioxidants caused no significant changes in the levels of neurotransmitters when administered alone to hamsters. However when administered with PA both carnosine and carnitine restored the altered neurotransmitters to near normal levels.ConclusionCarnosine and carnitine may be used as supplements to protect against PA neurotoxicity.
Highlights
Propionic acid (PA) occurs naturally in a few food products; for example PA is present in low quantities in milk and relatively higher levels in dairy products such as yogurt and cheese, obviously due to bacterial fermentation, mostly by propionibacteria [1,2]
Carnosine and carnitine may be used as supplements to protect against PA neurotoxicity
There are a series of inherited and acquired conditions which lead to elevations of PA and other short chain fatty acids and these are related to developmental delay, seizures and gastrointestinal symptoms, resembling some aspects of autism [22,23]
Summary
Propionic acid (PA) occurs naturally in a few food products; for example PA is present in low quantities in milk and relatively higher levels in dairy products such as yogurt and cheese, obviously due to bacterial fermentation, mostly by propionibacteria [1,2]. PA is a short chain fatty acid formed endogenously in the human body as an intermidiate of fatty acid metabolism and a metabolic end product of enteric gut bacteria such as clostridia and propionibacteria [3,5,6,7]. In this study hamsters were treated with the antibiotic clindamycin to see if its effects were similar to that of exogenous PA which has been implicated in autism. Propionic acid (PA) found in some foods and formed as a metabolic product of gut bacteria has been reported to mimic/mediate the effects of autism. The present study was undertaken to compare the effect of orally administered PA with that of clindamycin-induced PA-microbial producers in inducing persistent biochemical autistic features in hamsters. The neuroprotective potency of carnosine and carnitine supplements against PA toxicity was investigated
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