Soft-food diet induces oxidative stress in the rat brain
Highlights
► DA release in the hippocampus was reduced in the rats maintain on a soft-food diet. ► Soft-food diet feeding enhances oxidative stress in the rats. ► DA can directly scavenge ROS such as HO, and O2−.
Introduction
Mastication is thought to play an important role in both the promotion and prevention of senile dementia [24] and has recently been closely linked with brain function [22]. Our previous reports have shown that masticatory dysfunction induces deficits in spatial cognitive memory and a decrease in input activities in the rat hippocampus [23], [28]. Occlusal disharmonies and tooth loss cause degenerative changes in hippocampal neurons, a decrease in the number and density of septohippocampal cholinergic networks [13], [23], [27]. In rats fed a soft-food diet, the hippocampus shows decreased cell proliferation, neurogenesis [1], [19], [29].
Electron spin resonance (ESR) has been recognized as one of the most powerful techniques for the detection of free radicals in biological tissues and cells, and we have developed an ESR-based technique to evaluate oxidative stress in the brain [12], [15], [16]. Excessive levels of free radicals in the brain have been shown to be involved in several neurological disorders [3]. It is well known that free radicals, including reactive oxygen species (ROS) such as superoxide (O2−) or hydroxyl radical (HO), contribute to the development of several age-related diseases by causing oxidative stress. Oxidative stress is defined as an imbalance between pro-oxidants (e.g., ROS) and antioxidant defenses [9]. It has been suggested that 3-methoxycarbonyl-2,2,5,5-tetramethylpyrrolidine-1-oxyl (MC-PROXYL) is a suitable ESR spin probe for the study of oxidative stress in the brain [12], [15], [16]. In previous studies, using both ESR imaging and L-band ESR, we showed that masticatory motor activity movements, such as biting, suppress oxidative stress in the brain induced by restraint stress [21]. However, no previous studies have used ESR to measure the effects of soft- and hard-food diet on oxidative stress in the brain.
Using a rat model of Alzheimer's disease (AD), Kushida et al. demonstrated that animals fed soft-food diet had compromised hippocampal dopaminergic neuronal systems, which was linked with impaired learning and memory [14]. This result suggests that impairment of dopaminergic activity is related to the development of senile dementia and AD. However, the central mechanism by which dysfunctional mastication leads to a decrease in dopamine (DA) release in the hippocampus remains unclear. Thus, we investigated that the effects of soft- and hard-food diets on oxidative stress in the brain, and the relationship between these effects and hippocampal DA levels.
Section snippets
Materials and methods
Male Wistar rats were housed at 22 ± 3 C° under a 12-h light/dark cycle with free access to food and water. When the rats were 3 weeks old, feeding of a hard-food diet (MF solid, Oriental Yeast Co., Ltd., Osaka, Japan) or soft-food diet (MF powder, Oriental Yeast Co., Ltd., Osaka, Japan), which contained identical ingredients, was begun and was continued until the rats were 12 weeks old. The procedures used in this study were conducted in accordance with the guidelines of the US National Institute
Results
There were no significant differences in the basal level of extracellular DA in the hippocampus between the soft-food diet and hard-food diet groups (Fig. 1). In the soft-food diet group, extracellular DA release induced by perfusion of a high-K+ Ringer solution was decreased as compared with the hard-food diet group (Fig. 1).
L-band ESR was performed in rats after 12 weeks on the soft-food diet or hard-food diet. The metabolism of MC-PROXYL in isolated rat brain occurred in 2 phases, phase I
Discussion
The effects of a soft-food diet during development on subsequent oxidative stress in the adult hippocampus appears to be the result of chronic emotional stress and/or reduced masticatory muscle activity [17]. It has reported that one of the most effective promoters of tissue damage in the hippocampus is oxidative stress [25]. Our previous reports showed that oxidative stress in the rat brain was increased by restraint stress [20]. Oxidative stress has been shown to enhance tissue and DNA damage
Acknowledgements
This research was supported by a Grant-in-Aid for Scientific Research (Nos. 18592149, 19791469, 19592371, 20791622, 23593049, 23660047) from the Ministry of Education, Culture, Sports, Science and Technology of Japan.
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