Astaxanthin inhibits aldose reductase activity in <i>Psammomys obesus</i>, a model of type 2 diabetes and diabetic retinopathy

Khedher, Maha Benlarbi‐Ben; Hajri, Khouloud; Dellaa, Ahmed; Baccouche, Basma; Hammoum, Imane; Boudhrioua‐Mihoubi, Nourhene; Dhifi, Wissal; Chaouacha‐Chekir, Rafika Ben

doi:10.1002/fsn3.1259

Cited by 32 publications

(22 citation statements)

References 34 publications

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“…An inhibitory effect of ASX has also been recently reported on aldose reductase (AR) activity, a key enzyme in the polyol pathway involved in the pathogenesis of diabetic complications including DR in the gerbil (Gerbillidae family, Psammomys obesus species) animal models for T2DM [97]. In db/db mice, ASX improved oscillatory potentials (OPs) and the levels of OS markers including superoxide anion, MDA (a marker of lipid peroxidation), 8-hydroxy-2-deoxyguanosine (8-OHdG, indicator of oxidative DNA damage), and MnSOD (manganese superoxide dismutase) in the retinal tissue [98].…”

Section: Astaxanthin: Protection Against Diabetic Retinopathymentioning

confidence: 99%

Impact of Astaxanthin on Diabetes Pathogenesis and Chronic Complications

et al. 2020

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Oxidative stress (OS) plays a pivotal role in diabetes mellitus (DM) onset, progression, and chronic complications. Hyperglycemia-induced reactive oxygen species (ROS) have been shown to reduce insulin secretion from pancreatic β-cells, to impair insulin sensitivity and signaling in insulin-responsive tissues, and to alter endothelial cells function in both type 1 and type 2 DM. As a powerful antioxidant without side effects, astaxanthin (ASX), a xanthophyll carotenoid, has been suggested to contribute to the prevention and treatment of DM-associated pathologies. ASX reduces inflammation, OS, and apoptosis by regulating different OS pathways though the exact mechanism remains elusive. Based on several studies conducted on type 1 and type 2 DM animal models, orally or parenterally administrated ASX improves insulin resistance and insulin secretion; reduces hyperglycemia; and exerts protective effects against retinopathy, nephropathy, and neuropathy. However, more experimental support is needed to define conditions for its use. Moreover, its efficacy in diabetic patients is poorly explored. In the present review, we aimed to identify the up-to-date biological effects and underlying mechanisms of ASX on the ROS-induced DM-associated metabolic disorders and subsequent complications. The development of an in-depth research to better understand the biological mechanisms involved and to identify the most effective ASX dosage and route of administration is deemed necessary.

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Section: Astaxanthin: Protection Against Diabetic Retinopathymentioning

confidence: 99%

Impact of Astaxanthin on Diabetes Pathogenesis and Chronic Complications

et al. 2020

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“…Samples were fed with astaxanthin (4.8 mg/kg of body weight) once a day for one week. Results showed a marked reduction of AR activity in vivo and ex vivo following astaxanthin supplementation, thus supporting its role in both the prevention and early treatment of diabetic retinopathy [44].…”

Section: Retinal Diseasesmentioning

confidence: 63%

“…Then, the number of infiltrating cells and protein concentration in the aqueous humor collected 24 h after LPS treatment was determined. As a result, astaxanthin administration significantly decreased the production of NO, PGE2, and TNF-α by directly blocking NOS enzyme activity [44]. Interestingly, ocular anti-inflammatory effect of 100 mg/kg astaxanthin was comparable to that one of 10-mg/kg prednisolone [53].…”

Section: Uveitismentioning

confidence: 91%

“…Increased flux of polyol pathways, enhanced formation of advanced glycation end products (AGEs), upregulated hexosamine pathway and PKC activation result in the augmentation of oxidative agents, which then induce vascular dysfunction including membrane thickening, pericyte drop out and retinal capillary nonperfusion with subsequent retinal ganglion cell loss [16]. Starting from this assumption, the astaxanthin bioactive compound, which contains several double bonds to scavenge ROS, was shown to exert neuroprotective effects in several experimental models of diabetic retinopathy by reducing oxidative stress, inhibiting NF-κB activity and downregulating the expression of downstream inflammatory mediators, which act as principal stimuli of pathological CNV [16,44,45]. In the study by Yeh and coauthors, 50 female Wistar rats received an injection of streptozotocin (STZ) to induce diabetes and were then randomly selected into four groups that received daily for eight weeks: normal saline; 0.6 mg/kg astaxanthin; 3 mg/kg astaxanthin; 0.5 mg/kg lutein.…”

Section: Retinal Diseasesmentioning

confidence: 99%

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Clinical Applications of Astaxanthin in the Treatment of Ocular Diseases: Emerging Insights

et al. 2020

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Astaxanthin is a naturally occurring red carotenoid pigment belonging to the family of xanthophylls, and is typically found in marine environments, especially in microalgae and seafood such as salmonids, shrimps and lobsters. Due to its unique molecular structure, astaxanthin features some important biologic properties, mostly represented by strong antioxidant, anti-inflammatory and antiapoptotic activities. A growing body of evidence suggests that astaxanthin is efficacious in the prevention and treatment of several ocular diseases, ranging from the anterior to the posterior pole of the eye. Therefore, the present review aimed at providing a comprehensive evaluation of current clinical applications of astaxanthin in the management of ocular diseases. The efficacy of this carotenoid in the setting of retinal diseases, ocular surface disorders, uveitis, cataract and asthenopia is reported in numerous animal and human studies, which highlight its ability of modulating several metabolic pathways, subsequently restoring the cellular homeostatic balance. To maximize its multitarget therapeutic effects, further long-term clinical trials are warranted in order to define appropriate dosage, route of administration and exact composition of the final product.

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“…Astaxanthin from dietary sources is responsible for the orange-red coloration of salmon, lobster, and other seafood species, which cannot synthesize the compound de novo. Astaxanthin, particularly that from natural sources, is utilized extensively in the food, aquaculture, cosmetic, and pharmaceutical industries because of its distinctive coloration and antioxidant properties [1, [9][10][11][12].…”

Section: Introductionmentioning

confidence: 99%

Cell wall and cell membrane defects contribute to reduced cell growth at 28 °C in Phaffia rhodozyma mutant strain MK19

Miao

Chi

Hou

et al. 2020

Preprint

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Background: Phaffia rhodozyma has many desirable properties for astaxanthin production, including rapid heterotrophic metabolism and high cell densities in fermenter culture. The low optimal temperature range (17-21 °C) for cell growth and astaxanthin synthesis in this species presents an obstacle to efficient industrial-scale astaxanthin production. The inhibition mechanism of cell growth at > 21 °C in P. rhodozyma have not been investigated.Results: MK19, a mutant P. rhodozyma strain grows well at moderate temperatures, its cell growth was also inhibited at 28 °C, but such inhibition was mitigated, and low biomass 6 g/L was obtained after 100 h culture. Transcriptome analysis indicated that low biomass at 28 °C resulted from strong suppression of DNA and RNA synthesis in MK19. Growth inhibition at 28 °C was due to cell membrane damage with a characteristic of low mRNA content of fatty acid (f.a.) pathway genes (acc, fas1, fas2), and consequent low f.a. content. Thinning of cell wall and low mannose content (leading to loss of cell wall integrity) also contributed to reduced cell growth at 28 °C in MK19. Levels of astaxanthin and ergosterol, two end-products of isoprenoid biosynthesis (a shunt pathway of f.a. biosynthesis), reached 2000 μg/g and 7500 μg/g respectively; ~2-fold higher than levels at 21 or 25 °C. Abundance of ergosterol, an important cell membrane component, compensated for lack of f.a., making possible the biomass production of 6 g/L for MK19 at 28 °C. Conclusion: Inhibition of growth of P. rhodozyma at 28 °C results from blocking of DNA, RNA, f.a., and cell wall biosynthesis. In MK19, abundant ergosterol made possible biomass production 6 g/L at 28 °C. Significant accumulation of astaxanthin and ergosterol indicated a active MVA pathway in MK19 at 28 °C. Strengthening of the MVA pathway can be a feasible metabolic engineering approach for enhancement of astaxanthin synthesis in P. rhodozyma. The present findings provide useful mechanistic insights regarding adaptation of P. rhodozyma to 28 °C, and improved understanding of feasible metabolic engineering techniques for industrial scale astaxanthin production by this economically important yeast species.

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Astaxanthin inhibits aldose reductase activity in Psammomys obesus, a model of type 2 diabetes and diabetic retinopathy

Cited by 32 publications

References 34 publications

Impact of Astaxanthin on Diabetes Pathogenesis and Chronic Complications

Impact of Astaxanthin on Diabetes Pathogenesis and Chronic Complications

Clinical Applications of Astaxanthin in the Treatment of Ocular Diseases: Emerging Insights

Cell wall and cell membrane defects contribute to reduced cell growth at 28 °C in Phaffia rhodozyma mutant strain MK19

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