Dietary vitamin E deficiency increases anxiety-related behavior in rats under stress of social isolation

BioFactors ◽  
2009 ◽  
Vol 35 (3) ◽  
pp. 273-278 ◽  
Author(s):  
Yuki Okura ◽  
Satoshi Tawara ◽  
Takefumi Kikusui ◽  
Asako Takenaka
2020 ◽  
pp. 1-27
Author(s):  
Yuki Terada ◽  
Hiroya Ohashi ◽  
Yuki Otani ◽  
Kanako Tokunaga ◽  
Asako Takenaka

Abstract We previously reported that dietary vitamin E deficiency increased anxiety-like behavior in rats exposed to social isolation. Here, we performed a detailed investigation of this phenomenon and its underlying mechanism. First, we fed Wistar rats with vitamin E-free diet for 3 days, 1 week, or 2 weeks and found an increase in anxiety-like behavior after 1 and 2 weeks of vitamin E deficiency based on behavioral indicators. Next, we examined the effect of a control diet (150 mg all-racemic α-tocopherol acetate/kg) on anxiety-like behaviors in rats that received a 4- week vitamin E-free diet. We found that increased anxiety-like behavior was reversed to control levels after refeeding vitamin E for 7 days but not for 1 or 3 days. Further, anxiety-like behavior increased or decreased gradually based on the amount of vitamin E intake; however, it had a quicker progression than physical symptoms of vitamin E deficiency. Moreover, rats fed with excess vitamin E (500 mg all-racemic α-tocopherol/kg diet) showed less anxiety-like behavior than control rats, indicating that vitamin E supplementation is effective for preventing anxiety increase under social isolation stress. Since plasma corticosterone levels were higher in vitamin E deficient rats, we investigated the effect of adrenalectomy on anxiety-like behavior and found that adrenal hormones played an essential role in the increased anxiety-like behavior induced by vitamin E deficiency. In conclusion, increased anxiety-like behavior is a symptom that emerges earlier than physical vitamin E deficiency and is caused by adrenal hormone-dependent mechanisms.


Epidemiology ◽  
2006 ◽  
Vol 17 (Suppl) ◽  
pp. S249
Author(s):  
J Burns ◽  
D Dockery ◽  
L Neas ◽  
J Schwartz ◽  
B Coull ◽  
...  

2011 ◽  
Vol 75 (10) ◽  
pp. 1894-1899 ◽  
Author(s):  
Yuki TERADA ◽  
Yuki OKURA ◽  
Takefumi KIKUSUI ◽  
Asako TAKENAKA

Oncotarget ◽  
2016 ◽  
Vol 7 (51) ◽  
pp. 83869-83879 ◽  
Author(s):  
Kaiyu Wang ◽  
Erlong Wang ◽  
Zhenyang Qin ◽  
Zhen Zhou ◽  
Yi Geng ◽  
...  

1987 ◽  
Vol 247 (1) ◽  
pp. 135-140 ◽  
Author(s):  
Y Z Cao ◽  
K O ◽  
P C Choy ◽  
A C Chan

Lysophosphatidylcholine is the major lysophospholipid in mammalian tissues and has been shown to be cytolytic at high concentrations. In the present study we demonstrated that the level of lysophosphatidylcholine was significantly increased in the heart of rats fed with a vitamin E-deficient diet. Moreover, the cardiac lysophosphatidylcholine level was decreased in rats fed with a high vitamin E diet. The alterations in cardiac lysophosphatidylcholine level by dietary vitamin E were attributed to the changes in the activity of cardiac phospholipase A. Dietary vitamin E affected both phospholipase A1 and A2 in the same manner, but had no effect on the other major enzymes which are responsible for the metabolism of lysophosphatidylcholine. Kinetic studies revealed that the inhibition of enzyme activity by vitamin E was essentially non-competitive. The accumulation of lysophosphatidylcholine in the rat heart may be one of the underlying biochemical causes of the observed cardiac dysfunctions produced during vitamin E deficiency.


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