Abstract
α-tocopherol is a powerful liposoluble antioxidant and the most abundant isoform of vitamin E in the body. Under normal physiological conditions, adverse effects of relatively high concentration of vitamin E on organisms and the underlying mechanisms are still largely unclear. In the present study, we used the nematode Caenorhabditis elegans as an in vivo assay system to investigate the possible adverse effects of high concentration of vitamin E on thermosensation and thermotaxis learning and the underlying mechanisms. Our data show that treatment with 100–200 µg/mL of vitamin E did not noticeably influence both thermosensation and thermotaxis learning; however, treatment with 400 µg/mL of vitamin E altered both thermosensation and thermotaxis learning. The observed decrease in thermotaxis learning in 400 µg/mL of vitamin E treated nematodes might be partially due to the moderate but significant deficits in thermosensation, but not due to deficits in locomotion behavior or perception to food and starvation. Treatment with 400 µg/mL of vitamin E did not noticeably influence the morphology of GABAergic neurons, but significantly decreased fluorescent intensities of the cell bodies in AFD sensory neurons and AIY interneurons, required for thermosensation and thermotaxis learning control. Treatment with 400 µg/mL of vitamin E affected presynaptic function of neurons, but had no remarkable effects on postsynaptic function. Moreover, promotion of synaptic transmission by activating PKC-1 effectively retrieved deficits in both thermosensation and thermotaxis learning induced by 400 µg/mL of vitamin E. Therefore, relatively high concentrations of vitamin E administration may cause adverse effects on thermosensation and thermotaxis learning by inducing damage on the development of specific neurons and presynaptic function under normal physiological conditions in C. elegans.
Highlights
Vitamin E, a generic term for tocopherols and tocotrienols containing a group of eight lipid soluble substances with a chromanol ring and a saturated or unsaturated carbon side chain, has been widely studied for decades [1]
Treatment with 400 mg/mL of vitamin E significantly (p,0.01) decreased thermotaxis associative learning at the time intervals of 3, 12, and 18 hr compared with the control, thermotaxis learning behaviors at the time intervals of 0.5 hr and 1 hr in nematodes exposed to 400 mg/mL vitamin E were similar to those of the control (Fig. 1)
Because recording of the learning behavior in the used assay system may be influenced by thermosensation and locomotion behavior of the examined nematodes, we investigated the effects of vitamin E treatment at different concentrations on thermosensation in nematodes
Summary
Vitamin E, a generic term for tocopherols and tocotrienols containing a group of eight lipid soluble substances with a chromanol ring and a saturated or unsaturated carbon side chain, has been widely studied for decades [1]. Natural vitamin E has potent neuroprotective function against the neurotoxicity induced by toxicants such as manganese, homocysteic acid, linoleic acid, H2O2, polychlorinated biphenyls, pilocarpine, glutamate [2,3,4,5,6,7], and some diseases such as seizure and neurodegenerative diseases [5,8,9]. It has been shown that vitamin E can protect against cognitive and memory deficits induced by toxicants such as ozone, homocysteine, and ovariectomy and some diseases [10,11,12,13,14]. It has been proven that treatment with relatively high concentrations of vitamin was neurotoxic [4,17]. The underlying mechanisms for neurotoxicity from high concentrations of vitamin E are still unclear
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