Effects of ergothioneine on diabetic embryopathy in pregnant rats

Guijarro-Fuertes, Michelle; Indart, A.; Aruoma, Okezie I.; Viana, Marta; Bonet, Bartolomé

doi:10.1016/s0278-6915(02)00177-1

Cited by 29 publications

(14 citation statements)

References 18 publications

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“…Glucose levels in both pregnant and nonpregnant STZ-treated animals (Table 2) were significantly higher than in control groups (from 3-to 4-fold), in agreement with Guijarro et al (14). Due to our interest in the study of the embryos, mothers were not under fasting conditions at the moment they were killed to avoid alterations in the normal embryo development (1).…”

Section: Resultssupporting

confidence: 88%

Responses of mitochondrial biogenesis and function to maternal diabetes in rat embryo during the placentation period

Alcolea¹,

Lladó²,

García-Palmer³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Alcolea MP, Lladó I, García-Palmer FJ, Gianotti M. Responses of mitochondrial biogenesis and function to maternal diabetes in rat embryo during the placentation period. Am J Physiol Endocrinol Metab 293: E636-E644, 2007; doi:10.1152/ajpendo.00120.2007.-Mitochondria are cellular organelles that have been reported to be altered in diabetes, being closely related to its associated complications. Moreover, mitochondrial biogenesis and function are essential for proper embryo development throughout the placentation period, occurring during organogenesis, when a great rate of congenital malformations have been associated with diabetic pregnancy. Thus, the aim of the current work was to investigate the effect of the diabetic environment on mitochondrial function and biogenesis during the placentation period. For this purpose, we studied the oxidative phosphorylation system (OXPHOS) enzymatic activities as well as the expression of genes involved in the coordinated regulation of both mitochondrial and nuclear genome (PGC-1␣, NRF-1, NRF-2␣, mtSSB, and TFAM) and mitochondrial function (COX-IV, COX-I, and ␤-ATPase) in rat embryos from control and streptozotocininduced diabetic mothers. Our results reflected that diabetic pregnancy retarded and altered embryo growth. The embryos from diabetic mothers showing normal morphology presented a reduced content of proteins regulated through the PGC-1␣ mitochondriogenic pathway on gestational day 12. This fact was accompanied by several responses that entailed the activation of OXPHOS activities on the same day and the recovery of the content of the studied proteins to control levels on day 13. As a result, the mitochondria of these embryos would reach a situation close to control on day 13 that could allow them to follow the normal mitochondriogenic schedule throughout a gestational period in which the mitochondrial differentiation process is critical. Nevertheless, malformed embryos from diabetic mothers seemed to show a lower adaptation capability, which could exacerbate their maldevelopment.peroxisome proliferator-activated receptor-␥ coactivator-1␣; nuclear respiratory factors; mitochondrial transcription factor A; oxidative phosphorylation system THE ALTERED EMBRYO-FETAL DEVELOPMENT induced by the oxida-

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Section: Resultssupporting

confidence: 88%

Responses of mitochondrial biogenesis and function to maternal diabetes in rat embryo during the placentation period

Alcolea¹,

Lladó²,

García-Palmer³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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“…Probably such antioxidant activities are at the core of its biological benefits. Caenorhabditis elegans Protection from amyloid-β-induced cell death (521) Cell injury Rat pheochromocytoma cells Methylglyoxal challenge (573) Cell proliferation K562 cells Involvement of SLC22A4 (418) Caco-2 cells Involvement of SLC22A4 (429) Diabetic embryopathy Rats ERG reduced it to control levels (574) DNA damage in mitochondria HeLa, RAW 264•7, HaCaT, PC12 cells siRNA knockdown of SLC22A4…”

Section: The Biology Of Ergothioneinementioning

confidence: 99%

The biology of ergothioneine, an antioxidant nutraceutical

et al. 2020

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Ergothioneine (ERG) is an unusual thio-histidine betaine amino acid that has potent antioxidant activities. It is synthesised by a variety of microbes, especially fungi (including in mushroom fruiting bodies) and actinobacteria, but is not synthesised by plants and animals who acquire it via the soil and their diet, respectively. Animals have evolved a highly selective transporter for it, known as solute carrier family 22, member 4 (SLC22A4) in humans, signifying its importance, and ERG may even have the status of a vitamin. ERG accumulates differentially in various tissues, according to their expression of SLC22A4, favouring those such as erythrocytes that may be subject to oxidative stress. Mushroom or ERG consumption seems to provide significant prevention against oxidative stress in a large variety of systems. ERG seems to have strong cytoprotective status, and its concentration is lowered in a number of chronic inflammatory diseases. It has been passed as safe by regulatory agencies, and may have value as a nutraceutical and antioxidant more generally.

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“…Free radicalinduced DNA damage has been shown to be increased in embryos from diabetic rats [69] and what is more relevant is the fact that with the administration of vitamin E, the amount of DNA bases damaged by free radicals decreases to the levels observed in nondiabetic embryos [69] . Guijarro et al [70] further suggested that the coadministration of vitamin E with ergothioneine (a diet-derived antioxidant that does not itself have any effect on the plasma glucose levels, both in diabetic and control animals) significantly inhibits the glucose-mediated free radical-dependent embryo malformation. In addition, oxidative damage to DNA leads to the formation of fapyadenine which may arrest DNA polymerase [71] contributing significantly to the congenital malformations.…”

Section: Diabetic Embryopathymentioning

confidence: 99%

Free Radicals, Antioxidants and Diabetes: Embryopathy, Retinopathy, Neuropathy, Nephropathy and Cardiovascular Complications

et al. 2006

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The metabolic disturbances in the insulin-dependent diabetes mellitus or type 1 and noninsulin-dependent diabetes mellitus or type 2 are associated with a number of complications including cardiovascular diseases, nephropathy, neuropathy, retinopathy leading to blindness and embryopathy or congenital malformations. Maternal diabetes is associated with a high incidence of congenital malformations and fetal abortions. Heart and kidney anomalies, along with central nervous system defects are frequent manifestations of a maternal diabetic environment. Glycation products from excess glucose can chemically modify DNA causing mutations and complex DNA rearrangements. Therefore, DNA damage in fetal tissues as a result of maternal diabetes may reflect a level of genomic injury sufficient to affect embryonic development. The formation of advanced glycation end products can accelerate vascular occlusion by quenching the vasodilating agent nitric oxide. Interaction with high-affinity receptors located on monocytes and macrophages can enhance the production of free radicals and reactive oxygen/nitrogen species, the secretion of tumor necrosis factor-α, interleukin-1 and insulin-like growth factor 1 which can proliferate endothelial, mesangial and smooth muscle cells and hence contribute significantly to the pathogenesis of cardiovascular complications. Retinopathy is characterized by increased vascular permeability, by vascular closure, together with the growth of new blood vessels on the retina and posterior surface of the vitreous. Reactive oxygen species are involved in decreased retinal blood flow, increased vascular permeability and disruption of blood-retinal barrier. The involvement of oxidative stress in the pathology of diabetes from its associated cardiovascular dysfunctions, nephropathy, neuropathy, retinopathy (leading to blindness) and embryopathy or congenital malformations, suggests that potential management of diabetes could benefit from use of dietary biofactors in medicinal and food plants. There is therefore a requirement for research to focus on the molecular mechanisms of action of extracts and/or the biofactors flavonoids, proanthocyanidins, alkaloids, etc. derived from these plants.

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Effects of ergothioneine on diabetic embryopathy in pregnant rats

Cited by 29 publications

References 18 publications

Responses of mitochondrial biogenesis and function to maternal diabetes in rat embryo during the placentation period

Responses of mitochondrial biogenesis and function to maternal diabetes in rat embryo during the placentation period

The biology of ergothioneine, an antioxidant nutraceutical

Free Radicals, Antioxidants and Diabetes: Embryopathy, Retinopathy, Neuropathy, Nephropathy and Cardiovascular Complications

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