Elevation by Oxidative Stress and Aging of Hypothalamic-Pituitary-Adrenal Activity in Rats and Its Prevention by Vitamin E

Kobayashi, N.; Machida, Taiji; Takahashi, Takeyuki; Takatsu, Hirokatsu; Senoo, Tadashi; Abe, Kouichi; Urano, Shiro

doi:10.3164/jcbn.09-33

Cited by 39 publications

(29 citation statements)

References 26 publications

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“…Koji Fukui 1,6 , Hiroaki Kawakami 1 , Tatsuki Honjo 1 The purpose of this study was to determine whether vitamin E-deficient mice exhibit axonal degeneration or not. We focused on the hippocampal CA1 region, which plays an important role in cognitive function.…”

Section: Vitamin E Deficiency Induces Axonal Degeneration In Mouse Himentioning

confidence: 99%

“…One pivotal function of vitamin E is as an antioxidant (1), and vitamin E plays a role as a radical scavenger (2)(3)(4). Several lines of evidence demonstrate that vitamin E deficiency increases the risk of development and progression of serious diseases in human and animal models (5)(6)(7). For example, a vitamin E-deficient diet increased phospho-tau protein in mice expressing the human apolipoprotein E4 (5), and vitamin E-deficient rats exhibited hypersecretion of corticosterone, due to impairment of glucocorticosteroid receptors in the CA1 region of the hippocampus (6).…”

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confidence: 99%

“…Several lines of evidence demonstrate that vitamin E deficiency increases the risk of development and progression of serious diseases in human and animal models (5)(6)(7). For example, a vitamin E-deficient diet increased phospho-tau protein in mice expressing the human apolipoprotein E4 (5), and vitamin E-deficient rats exhibited hypersecretion of corticosterone, due to impairment of glucocorticosteroid receptors in the CA1 region of the hippocampus (6). Howard et al showed that severe a-tocopherol deficiency induced lethal myopathy in animal models (7).…”

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confidence: 99%

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Vitamin E Deficiency Induces Axonal Degeneration in Mouse Hippocampal Neurons

Fukui

Kawakami

Honjo

et al. 2012

J Nutr Sci Vitaminol

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SummarySeveral lines of evidence demonstrate the relationship between vitamin E deficiency and cognitive dysfunction in rodent models, but little is known about the underlying mechanisms. In this study, we found axonal injury in the hippocampal CA1 region of vitamin E-deficient and normal old mice using immunohistochemical assay. The number of cells in the hippocampal CA1 region of vitamin E-deficient mice and normal old mice was significantly lower than in normal young mice. It is well known that collapsin response mediator protein (CRMP)-2 plays a crucial role in the maintenance of axonal conditions. The expressions of CRMP-2 in the cerebral cortex and hippocampus of vitamin E-deficient mice were significantly lower than both the regions of normal ones. In normal old mice, the expression of CRMP-2 in the cerebral cortex was significantly lower than in the normal ones. In addition, the appearance of microtubule-associated protein (MAP)-light chain 3 (LC3), a major index of autophagy, was higher in the cerebral cortex and hippocampus of vitamin E-deficient mice than in normal young and old mice. These results indicate that axonal degeneration is induced in living tissues, but not cultured cells, and that changes in CRMP-2 and MAP-LC3 may underlie vitamin E-deficiency-related axonal degeneration.

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Section: Vitamin E Deficiency Induces Axonal Degeneration In Mouse Himentioning

confidence: 99%

mentioning

confidence: 99%

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confidence: 99%

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Vitamin E Deficiency Induces Axonal Degeneration in Mouse Hippocampal Neurons

Fukui

Kawakami

Honjo

et al. 2012

J Nutr Sci Vitaminol

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“…Similar phenomena were also observed in normal aged rats and young rats fed vitamin E-deficient diet kept in a normal atmosphere. Vitamin E supplementation prevented the decrease in glucocorticosteriod receptors in the hippocampus and the increase in corticosterone secretion caused by hyperoxia [35]. All these parameters are giving positive response towards antioxidant therapy.…”

Section: Resultsmentioning

confidence: 89%

Effect of Ubiquinol on Serum Reproductive Hormones of Amenorrhic Patients

Thakur¹,

Littaru

Funahashi

et al. 2015

Ind J Clin Biochem

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In neuroendocrine system the increase in oxidative status is produced by a glucocorticoid-dependent and transcriptional increase in pro-oxidative drive, with concurrent inhibition of the antioxidant defense system, ultimately leading to increased neuronal cell death. Functional hypothalamic disturbances and neuroendocirne aberrations have both short and long term consequences for reproductive health. Understandably, an impaired or diminished hypothalamic-pituitary-ovarian axis leads to anovulation and hypoestrogenism. Anovulation is directly linked to the neurohormonal and hormonal background of Functional Hypothalamic Amenorrhea. Impairment of pulsatile Gonadotropin Releasing Hormone secretion causes the impairment of pulsatile Lutenizing Hormone (LH) and Follicle Stimulating Hormone (FSH) secretion. The importance of oxidative stress in various pituitary disorders suggesting a possible clinical usefulness of antioxidant molecules like the lipophilic antioxidant Ubiquinol. Coenzyme Q10 or Ubiquinol is an essential part of the cell energy-producing system of mitochondria. However, it is also a powerful lipophilic antioxidant, protecting lipoproteins and cell membranes from autooxidation. Due to these unique actions Ubiquinol is used in clinical practice as an antioxidants for neurodegenerative diseases. So to identify the role of Ubiquinol on reproductive hormones FSH and LH, we have included 50 infertile patients of age group of 20-40, which are mostly amenorrhic. Out of 50 only 30 patients were in continuous follow up after supplementing them with 150 mg of Ubiquinol every day for 4 months. The hormonal levels were estimated by Enzyme Linked Immuno Sorbent Assay technique at follicular phase. The result suggests that FSH concentration is increased up to three times (from 3.10 ± 2.70 to 10.09 ± 6.93) but remains within the normal limit (P \ 0.05). LH values were found doubled (P \ 0.05) than its normal range (from 14.83 ± 10.48 to 27.85 ± 22.30). The Prolactin values were decreased while Progesterone values were high but not in the significant range (P [ 0.05). The supplementation of 150 mg of Ubiquinol may reduce the oxidative stress in neuroendocrine system which further improves the function of diminished HPA axis. Hence increased level of FSH and LH may be due to reduced oxidative stress by Ubiquinol.

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“…For example, chronic oxidative damage has been implicated in the aging process through the production of reactive oxygen species (ROS) that in turn produce lipid peroxidation and damage to tissues, in particular lipidrich ones, such as the central nervous system. Thus, oxidative stress mimics the effects of aging on cognitive impairment and antioxidant treatment with vitamin E (VE; α-tocopherol) can prevent or delay the damage [5][6][7] . At least part of the brain tissue damage produced by H or HI may be caused by oxidative stress that originated in the reperfusion process [8,9] .…”

Section: Introductionmentioning

confidence: 99%

Reversion by Vitamin E Treatment of the Oxidative Damage but Not of the Advancement in Reproductive Senescence Produced by Neonatal Hypoxia or Hypoxia-Ischemia in Female Rats

et al. 2014

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Background/Aims: Few studies address the long-term consequences of perinatal hypoxia (H), a frequent birth complication. Previously we described advanced reproductive senescence (premature loss of regular cyclicity) in female rats subjected to perinatal H or H plus unilateral ischemia (HI) associated with changes in the hypothalamic expression of estrogen and opioid receptors. Our aim is to explore whether hypothalamic inflammation and oxidative damage mediate these reproductive alterations. Methods: Female rats were subjected on postnatal day (PND) 7 to H (6.5% O₂ for 50 min) or HI (H + right carotid artery ligature) and inflammation/oxidative damage markers, such as iNOS, nNOS, insulin-like growth factor (IGF) system expression, glial reaction and macrophage invasion in the medial basal hypothalamus-preoptic area (GFAP Western blot and immunohistochemistry, ED1 immunohistochemistry), were determined. The effect of antioxidant treatment with vitamin E (VE; 1.5 mg/rat on PND 4, 6 and 8) was also explored. Results: No significant cellular inflammatory reactions were observed although GFAP protein was significantly increased at early times after injury. Forty-eight hours after injury iNOS, nNOS and IGF-I mRNA decreased in the HI group, and nNOS in the H group. IGFBP-3 mRNA increased in HI rats at 48 h and 30 days, while it fell at 7 days postinjury in both groups. VE treatment prevented the effects of HI on oxidation/inflammation markers, but did not prevent the premature onset of reproductive senescence or the altered hormone receptors expression. Conclusion: These results suggest that the oxidative and inflammatory damage caused by perinatal H or HI may not be responsible for the late-onset reproductive abnormalities.

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Elevation by Oxidative Stress and Aging of Hypothalamic-Pituitary-Adrenal Activity in Rats and Its Prevention by Vitamin E

Cited by 39 publications

References 26 publications

Vitamin E Deficiency Induces Axonal Degeneration in Mouse Hippocampal Neurons

Vitamin E Deficiency Induces Axonal Degeneration in Mouse Hippocampal Neurons

Effect of Ubiquinol on Serum Reproductive Hormones of Amenorrhic Patients

Reversion by Vitamin E Treatment of the Oxidative Damage but Not of the Advancement in Reproductive Senescence Produced by Neonatal Hypoxia or Hypoxia-Ischemia in Female Rats

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