Effects of D-allulose on di (2-ethylhexyl) phthalate (DEHP) and di-n-butyl phthalate (DBP)-induced toxicity in rats

Abstract

Background: Oral exposure to high concentrations of DEHP and DBP causes testicular and hepatotoxicity in rodents. Phthalate metabolites such as mono (2-ethylhexyl) phthalate (MEHP) and mono-n-butyl phthalate (MBP) stimulate peroxisome proliferator-activated receptors and disrupts carbohydrate and lipid metabolism. The oxidative stress generated may be closely related to these toxicities. Method: To clarify the effects of the rare sugar D-allulose, a potent free radical scavenger, on testicular and hepatotoxicity induced by DEHP and DBP, rats were fed DEHP or DBP containing diet and D-allulose water. Result: Dietary exposure to DEHP and DBP induced a significant decrease in testicular weight and significant increase in liver weight. D-allulose treatment significantly inhibited the testicular weight loss. But D-allulose treatment did not significantly suppress the increase in liver weight. Plasma glucose levels were significantly lower in the DEHP- or DBP-only treated groups compared to controls, but were improved by D-allulose treatment. This suggests that D-allulose blocks DEHP- and DBP-induced glycemic suppression. Plasma lipid-related markers such as total cholesterol, high-density lipoprotein cholesterol, and triglycerides were lower than controls in all treatment groups on the DEHP and DBP diets, but showed a slight trend toward improvement with D-allulose. Conclusion: D-allulose reduced DEHP- and DBP-induced testicular toxicity and blood glucose suppression in rats, but did not improve liver hypertrophy. This effect may be due to the strong oxidant scavenging ability of D-allulose.