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Colonization by toxin-producing bacteria in the gut plays a major role in bowel problems in autistic patients. Prebiotics can inhibit the growth of these pathogenic microbes by nourishing beneficial bacteria, while probiotics--live microorganisms--can balance the gut bacteria; thus, both together can maintain healthy bacteria in the gut. The present study was conducted to find the effect of probiotics and prebiotics in balancing the gut flora in a rodent model of autism linked with a clindamycin-induced altered gut. The effects of probiotics and prebiotics on oxidative stress markers in the brain were also evaluated. Eight groups of hamsters were assigned, with Group I serving as the control; Group II, as the autistic model, was treated with 250 mg propionic acid/kg BW/day for 3 days; Group III was treated with clindamycin 30 mg/kg BW for 3 days; Groups IV and V were treated with bee pollen and propolis (supposed prebiotics) at a dose of 250 mg/kg BW/day for 28 days; Group VI and Group VII were treated with Lactobacillus paracaseii and Protexin® (supposed probiotics) for 28 days; and finally, Group VIII was anorectally transplanted with stool from normal animals for 5 days. Remarkable changes were measured in oxidative stress markers, primarily glutathione and vitamin C, in the brains of hamsters in the propionic acid- and clindamycin-treated group. All probiotic/prebiotic treatments showed ameliorative effects; however, lactobacillus had the strongest effect. We conclude that pro-and prebiotic supplements may be effective to revive healthy digestive system function in autistic patients. The disappointing results of the fecal transplants suggest that further study is needed to develop an appropriate technique.

Propionic acid (PA) is a short chain fatty acid, a common food preservative and metabolic end product of enteric bacteria in the gut. The present study was undertaken to investigate the effect of PA on liver injury in male rats. Male western albino rats were divided into two groups. The first group served as normal control, the second was treated with PA. The activities of serum hepatospecific markers such as aspartate transaminase, alanine transaminase, and alkaline phosphatase were estimated. Antioxidant status in liver tissues was estimated by determining the level of lipid peroxidation and activities of enzymatic and non-enzymatic antioxidants. Sodium and potassium levels were also measured in liver tissue. PA treatment caused significant changes in all hepatospecific markers. Biochemical analysis of liver homogenates from PA-treated rats showed an increase in oxidative stress markers like lipid peroxidation and lactate dehydrogenase, coupled with a decrease in glutathione, vitamin C and glutathione S- transferase. However, PA exposure caused no change in sodium and potassium levels in liver tissue. Our study demonstrated that PA persuade hepatic damage in rats.