Effect of chronic γ-irradiation and β-carotene on lipid metabolism in presynaptic membranes in rat brain

2000 ◽  
Vol 129 (6) ◽  
pp. 533-536
Author(s):  
I. K. Kolomiitseva ◽  
N. I. Potekhina ◽  
T. P. Semenova ◽  
N. I. Medvinskaya ◽  
V. I. Popov ◽  
...  
1998 ◽  
Vol 126 (3) ◽  
pp. 918-920
Author(s):  
T. P. Kulagina ◽  
S. A. Shuruta ◽  
I. K. Kolomiitseva ◽  
L. A. Vakulova

2007 ◽  
Vol 282 (46) ◽  
pp. 33553-33561 ◽  
Author(s):  
Susanne Hessel ◽  
Anne Eichinger ◽  
Andrea Isken ◽  
Jaume Amengual ◽  
Silke Hunzelmann ◽  
...  

Carotenoids are currently investigated regarding their potential to lower the risk of chronic disease and to combat vitamin A deficiency in humans. These plant-derived compounds must be cleaved and metabolically converted by intrinsic carotenoid oxygenases to support the panoply of vitamin A-dependent physiological processes. Two different carotenoid-cleaving enzymes were identified in mammals, the classical carotenoid-15,15′-oxygenase (CMO1) and a putative carotenoid-9′,10′-oxygenase (CMO2). To analyze the role of CMO1 in mammalian physiology, here we disrupted the corresponding gene by targeted homologous recombination in mice. On a diet providing β-carotene as major vitamin A precursor, vitamin A levels fell dramatically in several tissues examined. Instead, this mouse mutant accumulated the provitamin in large quantities (e.g. as seen by an orange coloring of adipose tissues). Besides impairments in β-carotene metabolism, CMO1 deficiency more generally interfered with lipid homeostasis. Even on a vitamin A-sufficient chow, CMO1-/- mice developed a fatty liver and displayed altered serum lipid levels with elevated serum unesterified fatty acids. Additionally, this mouse mutant was more susceptible to high fat diet-induced impairments in fatty acid metabolism. Quantitative reverse transcription-PCR analysis revealed that the expression of peroxisome proliferator-activated receptor γ-regulated marker genes related to adipogenesis was elevated in visceral adipose tissues. Thus, our study identifies CMO1 as the key enzyme for vitamin A production and provides evidence for a role of carotenoids as more general regulators of lipid metabolism.


2015 ◽  
Vol 572 ◽  
pp. 11-18 ◽  
Author(s):  
Youn-Kyung Kim ◽  
Michael V. Zuccaro ◽  
Brianna K. Costabile ◽  
Rebeka Rodas ◽  
Loredana Quadro

Author(s):  
И. Беляев ◽  
I. Belyaev ◽  
А. Самойлов ◽  
A. Samoylov

Purpose: Experimental evaluation of β-carotene correction of radiation induced by single acute γ-irradiation of spermatogenesis disorders in male (♂) F1 CBAxC97Bl mice and non-linear rats with short-term carotenoid prescription. Material and methods: Single external gamma irradiation ♂ was performed at the IGUR facility (137Cs, dose rate 0.029 Gy/s). The β-carotene suspension was administered ♂ orally 19 and 4 hours before, 4 and 24 hours after irradiation. The damage and effectiveness of protection of spermatogenesis of irradiated ♂ were judged by the state of their reproductive function. Results: The effects of correction of the short-term prescription of β-carotene radiation-induced by a single acute external gamma irradiation at doses of 3 and 5 Gy of spermatogenesis disorders in mice and rats at stages of mature spermatozoa, spermatids and spermatogonium have been established. β-carotene in ♂ mice reduced total embryonic mortality in 8–14 and 77–84 days after irradiation at a dose of 3 Gy from 46 to 36 and from 41 to 28 %, preimplantation – after 8–14 and 15–21 days – from 24 up to 13 and from 31 to 22 %, postimplantation – after 0–7 and 77–84 days – from 24 to 15 and from 25 to 7 %. In ♂ rats 0–7 days after irradiation at a dose of 5 Gy β-carotene reduced total, pre-, post- and induced postimplantation embryonic mortality from 62 to 41, from 34 to 17, from 41 to 30 and from 38 to 26 %, respectively. After 13–20 days – preimplantation mortality from 27 to 11 %. At the stage of spermatozoa after irradiation at a dose of 3 Gy increased the breeding efficiency from 70 to 100 %, fecundity – by 23–31 %; reduced total and preimplantation mortality from 49 to 39 % and from 41 to 27 %, respectively. At the stage of spermatids –sterilization was prevented and the efficiency of breeding was normalized, reduced post- and induced postimplantation mortality from 25 to 20 and from 17 to 12 %, respectively. The therapeutic and prophylactic effects of β-carotene at the spermatocyte stage are not revealed. In the spermatogonium stage, the carotenoid increased the total number and number of live embryos in pregnant female (♀) from 36 to 55 and from 20 to 50 %, reduced total and pre-implantation mortality from 81 to 56 and from 69 to 42 %, respectively. Conclusions: The prospects of β-carotene use for correction of gonadal radiation injuries in the risk groups of exposure to ionizing radiation and the inclusion of β-carotene in the scheme of drug prevention of acute radiation injuries of spermatogenesis are shown.


2004 ◽  
Vol 24 (12) ◽  
pp. 1011-1021 ◽  
Author(s):  
Jung Sook Seo ◽  
Kyeung Soon Lee ◽  
Jung Hyun Jang ◽  
Zhejiu Quan ◽  
Kyung Mi Yang ◽  
...  

2014 ◽  
Vol 307 (11) ◽  
pp. H1675-H1684 ◽  
Author(s):  
Seung-Ah Lee ◽  
Hongfeng Jiang ◽  
Chad M. Trent ◽  
Jason J. Yuen ◽  
Sureshbabu Narayanasamy ◽  
...  

Dietary carotenoids like β-carotene are converted within the body either to retinoid, via β-carotene-15,15′-dioxygenase (BCO1), or to β-apo-carotenoids, via β-carotene-9′,10′-oxygenase 2. Some β-apo-carotenoids are potent antagonists of retinoic acid receptor (RAR)-mediated transcriptional regulation, which is required to ensure normal heart development and functions. We established liquid chromatography tandem mass spectrometery methods for measuring concentrations of 10 β-apo-carotenoids in mouse plasma, liver, and heart and assessed how these are influenced by Bco1 deficiency and β-carotene intake. Surprisingly, Bco1−/− mice had an increase in heart levels of retinol, nonesterified fatty acids, and ceramides and a decrease in heart triglycerides. These lipid changes were accompanied by elevations in levels of genes important to retinoid metabolism, specifically retinol dehydrogenase 10 and retinol-binding protein 4, as well as genes involved in lipid metabolism, including peroxisome proliferator-activated receptor-γ, lipoprotein lipase, Cd36, stearoyl-CoA desaturase 1, and fatty acid synthase. We also obtained evidence of compromised heart function, as assessed by two-dimensional echocardiography, in Bco1−/− mice. However, the total absence of Bco1 did not substantially affect β-apo-carotenoid concentrations in the heart. β-Carotene administration to matched Bco1−/− and wild-type mice elevated total β-apo-carotenal levels in the heart, liver, and plasma and total β-apo-carotenoic acid levels in the liver. Thus, BCO1 modulates heart metabolism and function, possibly by altering levels of cofactors required for the actions of nuclear hormone receptors.


2021 ◽  
Vol 118 (5) ◽  
pp. 2043-2052
Author(s):  
Yijin Zhao ◽  
Yueping Zhang ◽  
Jens Nielsen ◽  
Zihe Liu

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