Comparative Effects of Non-Gelatinized Corn and Rice Starches on the Life-Span of ICR Mice

Yamaki, Kohji; Ishii, Takashi; Takano-Ishikawa, Yuko; Shinohara, Kazuki

doi:10.1271/bbb.69.13

Cited by 3 publications

(1 citation statement)

References 21 publications

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“…11,29 Therefore, cellular protection systems, especially antioxidant systems, detoxification systems, molecular chaperones and protein degradation systems, play a pivotal role in the aging process, and the decline of cytoprotection results in accumulation of oxidative damage thus facilitating the aging process. 8,[31][32][33][34] The mean survival rate of the male ICR mice was assessed about 20 months, 35 so it is premised that 9-months and 11-months old are middle age in male ICR mice. Liver is the primary metabolism and detoxification organ, which is intimately associated with the aging process.…”

Section: The Sfps Ameliorates Oxidative Stress Induced By D-galactosementioning

confidence: 99%

Sargassum fusiforme polysaccharides activate antioxidant defense by promoting Nrf2-dependent cytoprotection and ameliorate stress insult during aging

Chen

et al. 2016

Food Funct.

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Aging is a complex issue, which results in a progressive decline process in cellular protection and physiological functions. Illustrating the causes of aging and pharmaceutical interference with the aging process has been a pivotal issue for thousands of years. Sargassum fusiforme (S. fusiforme), a kind of brown alga, is also named the "longevity vegetable" as it is not only a kind of food, but also used as an herb in traditional Chinese Medicine for maintaining health and treatment of thyroid disease, cardiovascular disease and so on. But how S. fusiforme promotes longevity is vastly equivocal. We got clues from S. fusiforme polysaccharides, which exhibited antioxidant activity, but the underlying mechanisms remained unclear. In this study, we evaluated the antioxidant effect and the possible mechanisms that S. fusiforme polysaccharides have against d-galactose-induced aging and chronic aging. We selected the SFPS as the candidate for antioxidant defense evaluation, which is a type of S. fusiforme polysaccharide with strong free radical scavenging activity and non-toxicity. It revealed that the antioxidant defense of the d-galactose-induced mice was markedly recovered when they were intragastrically administrated with the SFPS. However, oxidative damage may not be the only cause of aging. We further evaluated the function of the SFPS in the chronic aging mice. Intriguingly, we even found an obvious aging phenotype in the middle aged male ICR mice, which showed a significant decline in Nrf2-dependent cytoprotection. When 9-month old male ICR mice were treated with the SFPS for 2 months or even 11 months to their mean survival age, experimental measurements showed that the SFPS significantly promoted the antioxidant defense and mitochondrial integrity during aging. Furthermore, we suggest that the SFPS promotes Nrf2-dependent cytoprotection by upregulating the nuclear Nrf2 translocation, which may be mediated by p21 and JNK dependent pathways. These results suggest that the SFPS may decelerate the aging process by enhancing Nrf2-dependent cytoprotection, especially antioxidant defense.

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Section: The Sfps Ameliorates Oxidative Stress Induced By D-galactosementioning

confidence: 99%

Sargassum fusiforme polysaccharides activate antioxidant defense by promoting Nrf2-dependent cytoprotection and ameliorate stress insult during aging

Chen

et al. 2016

Food Funct.

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Carbohydrate restriction does not change mitochondrial free radical generation and oxidative DNA damage

Sanz

Gómez

Caro

et al. 2006

J Bioenerg Biomembr

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Many previous investigations have consistently reported that caloric restriction (40%), which increases maximum longevity, decreases mitochondrial reactive species (ROS) generation and oxidative damage to mitochondrial DNA (mtDNA) in laboratory rodents. These decreases take place in rat liver after only seven weeks of caloric restriction. Moreover, it has been found that seven weeks of 40% protein restriction, independently of caloric restriction, also decrease these two parameters, whereas they are not changed after seven weeks of 40% lipid restriction. This is interesting since it is known that protein restriction can extend longevity in rodents, whereas lipid restriction does not have such effect. However, before concluding that the ameliorating effects of caloric restriction on mitochondrial oxidative stress are due to restriction in protein intake, studies on the third energetic component of the diet, carbohydrates, are needed. In the present study, using semipurified diets, the carbohydrate ingestion of male Wistar rats was decreased by 40% below controls without changing the level of intake of the other dietary components. After seven weeks of treatment the liver mitochondria of the carbohydrate restricted animals did not show changes in the rate of mitochondrial ROS production, mitochondrial oxygen consumption or percent free radical leak with any substrate (complex I- or complex II-linked) studied. In agreement with this, the levels of oxidative damage in hepatic mtDNA and nuclear DNA were not modified in carbohydrate restricted animals. Oxidative damage in mtDNA was one order of magnitude higher than that in nuclear DNA in both dietary groups. These results, together with previous ones, discard lipids and carbohydrates, and indicate that the lowered ingestion of dietary proteins is responsible for the decrease in mitochondrial ROS production and oxidative damage in mtDNA that occurs during caloric restriction.

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Lipopolysaccaride-Induced Neutrophilic Inflammation in the Lungs Differs With Age

Ito

Betsuyaku

Nasuhara

et al. 2007

Experimental Lung Research

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In aged humans and animals, lung injuries are generally more serious and prolonged. From a kinetic perspective, the authors thus assessed whether lung expression of proinflammatory cytokines were altered with age following intratracheal lipopolysaccharide (LPS) challenge in mice. Tumor necrosis factor-alpha, interleukin-1beta, macrophage inflammatory protein-1alpha, macrophage inflammatory protein-2, and keratinocyte-derived chemokine were significantly higher in 65-week-old mice along with sustained neutrophilia when compared to 11-week-old mice at 72 hours, but not at earlier time points. The authors concluded that the degree of LPS-induced neutrophilic inflammation and the expression of these cytokines differ with age at later phases of acute lung injury.

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Comparative Effects of Non-Gelatinized Corn and Rice Starches on the Life-Span of ICR Mice

Cited by 3 publications

References 21 publications

Sargassum fusiforme polysaccharides activate antioxidant defense by promoting Nrf2-dependent cytoprotection and ameliorate stress insult during aging

Sargassum fusiforme polysaccharides activate antioxidant defense by promoting Nrf2-dependent cytoprotection and ameliorate stress insult during aging

Carbohydrate restriction does not change mitochondrial free radical generation and oxidative DNA damage

Lipopolysaccaride-Induced Neutrophilic Inflammation in the Lungs Differs With Age

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