Abstract
Diisononyl phthalate (DINP) is a plasticizer that is frequently used as a substitute for other plasticizers whose use is prohibited in certain products. In vivo studies on the neurotoxicity of DINP are however, limited. This work aims to investigate whether DINP causes neurobehavioral changes in mice and to provide useful advice on preventing the occurrence of these adverse effects. Behavioral analysis showed that oral administration of 20 or 200 mg/kg/day DINP led to mouse cognitive deficits and anxiety. Brain histopathological observations, immunohistochemistry assays (cysteine-aspartic acid protease 3 [caspase-3], glial fibrillary acidic protein [GFAP]), oxidative stress assessments (reactive oxygen species [ROS], glutathione [GSH], superoxide dismutase [SOD] activities, 8-hydroxy-2-deoxyguanosine [8-OH-dG] and DNA-protein crosslinks [DPC]), and assessment of inflammation (tumor necrosis factor alpha [TNF-а] and interleukin-1 beta [IL-1β]) of mouse brains showed that there were histopathological alterations in the brain and increased levels of oxidative stress, and inflammation for these same groups. However, some of these effects were blocked by administration of melatonin (50 mg/kg/day). Down-regulation of oxidative stress was proposed to explain the neuroprotective effects of melatonin. The data suggests that DINP could cause cognitive deficits and anxiety in mice, and that melatonin could be used to avoid these adverse effects.
Highlights
Restrictions on the use of DEHP, DBP and BzBP in consumer products
The mice received no training on the 13th day, and the spatial memory ability of the mice after diisononyl phthalate (DINP) exposure was evaluated on the 14th day
DINP has been widely used as a substitute for DEHP by the chemical industry in the manufacture of polymers and a variety of consumer products
Summary
Restrictions on the use of DEHP, DBP and BzBP in consumer products These regulations have resulted in the replacement of DEHP, DBP and BzBP with other less toxic phthalates, especially diisononyl phthalate (DINP)[6]. Humans may be exposed to DINP via oral, dermal, and inhalation routes. DINP is regarded as a less toxic phthalate, the adverse health effects, including reproductive toxicity, organ toxicity, and carcinogenicity have been observed in previous studies. There are some studies into the toxic effects resulting from exposure to DINP, neurotoxicity data are limited. After mice were orally exposed to DINP (0 mg/kg/day, 0.2 mg/kg/day, 2 mg/kg/day, 20 mg/kg/ day, 200 mg/kg/day), we looked for behavioral changes using the Morris water maze [MWM] test and the Open field test [OFT], and tested for brain tissue damage using histopathological observations and immunohistochemistry assays. The primary goal of this work was to define any damage in the mouse brain after exposure to DINP, and to investigate whether melatonin could be used as an agent to protect against high doses of DINP (Fig. 1)
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