Lutein effect on retina and hippocampus of diabetic mice

Muriach, Marí­a; Bosch‐Morell, Francisco; Alexander, G.; Blomhoff, Rune; Barcia, Jorge M.; Arnal, Emma; Almansa, Inmaculada; Romero, Francisco J.; Miranda, María

doi:10.1016/j.freeradbiomed.2006.06.023

Cited by 99 publications

(98 citation statements)

References 27 publications

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“…lutein has been shown to attenuate oxidative stress in experimental models of early diabetic retinopathy (17,18) . A role for lycopene in ocular health is also plausible; lycopene is present in high concentrations in human ocular tissues (19) , is the most potent carotenoid quencher of singlet oxygen (20) , and has other important functions.…”

Section: Discussionmentioning

confidence: 99%

Plasma carotenoids and diabetic retinopathy

et al. 2008

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Diabetic retinopathy increases with duration of diabetes and may be associated with carotenoid status. Carotenoids alter the pro-oxidation/antioxidation balance, and circulating levels depend largely on dietary intake. Lower levels have been reported in diabetes and age-related macular degeneration; however, little is known of the relationship between carotenoids and diabetic complications. Consequently, the purpose of the present study was to evaluate the relationship between plasma carotenoids and diabetic retinopathy. We assessed the carotenoid -retinopathy relationship in 111 individuals with type 2 diabetes in a community-based, cross-sectional study. We photodocumented retinal status and used HPLC to measure plasma carotenoid concentrations. Data for clinical and demographic variables and risk factors for diabetic retinopathy were obtained from 24 h urine and fasting blood samples, and an interviewer-assisted lifestyle questionnaire. We found that the combined lycopene and lutein/zeaxanthin (non-pro-vitamin A (non-PVA) carotenoid) concentration when compared with the pro-vitamin A (PVA) carotenoids (a-carotene, b-carotene and b-cryptoxanthin) was significantly lower in the retinopathy than non-retinopathy group (OR 1·2 (95 % CI 1·0, 1·4) v. 1·6 (95 % CI 1·4, 1·7), respectively; P¼0·009). A higher non-PVA:PVA ratio also predicted a lower risk of diabetic retinopathy, after adjustment for potential confounders (OR 0·33 (95 % CI 0·12, 0·95); P¼0·039). Finally, a higher concentration of PVA carotenoids was associated with greater odds of diabetic retinopathy, after adjustment for risk factors (P¼ 0·049). We suggest synergies between carotenoids are implicated in diabetic retinopathy, independent of established risk factors. Importantly, our observations indicate dietary modulation of retinopathy risk may be possible by increasing intakes of lutein-and lycopene-rich foods. Carotenoids: Diabetic retinopathy: Pro-vitamin ACarotenoids demonstrate a vast array of biological activities, including vital roles in the eye, both functionally as precursors to retinol in the visual pathway (pro-vitamin A (PVA) carotenoids) and structurally as macular pigments. The major PVA carotenoids in plasma are a-carotene, b-carotene and b-cryptoxanthin. Of these, only b-carotene is found in ocular tissues (1) .In contrast, lutein/zeaxanthin and lycopene are the major non-PVA carotenoids, i.e. are not retinol precursors, and both are present in ocular tissues at high concentrations. Lutein and zeaxanthin comprise the macular pigments, essential for normal vision and for the protection of photoreceptors from phototoxic blue light, while lycopene is present in high concentrations in the human ciliary body and retinal pigment epithelium/choroid (2) .Plasma carotenoid concentrations have been linked to numerous conditions (3 -6) including the major blinding conditions -age-related macular degeneration (7,8) and cataracts (9) . To date, the relationship between the major carotenoids and diabetic retinopathy has not been evaluated (Table ...

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Section: Discussionmentioning

confidence: 99%

Plasma carotenoids and diabetic retinopathy

et al. 2008

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“…At 24 h, 1 week or 4 weeks after treatments, retinal function was assessed by electroretinography (ERG), as previously described [22,23] . After overnight dark adaptation, rats were anesthetized as above, anesthetic and mydriatic collyrium were administered, and ERG was performed under dim red light.…”

Section: Electroretinogrammentioning

confidence: 99%

Transient Bevacizumab (Avastin)-Induced Alterations in Rat Eyes

Sancho‐Tello¹,

Johnsen-Soriano²,

Muriach

et al. 2008

Ophthalmic Res

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Aims: To study the histopathological, biochemical and functional effects of intravitreal bevacizumab on the rat eye, with special emphasis on its immediate pro-inflammatory features eventually associated with cellular oxidative burden. Methods: Histopathological evaluation was performed 24 h, 1 and 4 weeks after bevacizumab (75 μg/rat eye) or saline intravitreal injection, as well as biochemical analysis of oxidative stress-related markers and electroretinograms. Results: Bevacizumab induces a transient inflammatory reaction together with a modification of the b-wave amplitude and latency of the electroretinogram. No changes were observed in any of the oxidative stress markers studied at any time after injection. Conclusion: Intravitreal bevacizumab injection per se generates an immediate, transient and mild inflammation of the rat eye, which is not associated with oxidative stress in ocular tissues.

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“…The reduction of free radicals and oxidative stress through the administration of lutein (Dilsiz et al, 2006;Li et al, 2009) During the past decade, numerous studies have investigated neuroprotective strategies to reduce / prevent retinal cell death. Recently, intensive efforts have been made to explicate the neuroprotective effects of carotenoids in ocular diseases in vivo (Li et al, 2009;Muriach et al, 2006;Sasaki et al, 2009) and in vitro (Li and Lo, 2010;Nakajima et al, 2009). Various carotenoids are present in human plasma, but only the xanthophylls lutein and zeaxanthin are found in retina in considerable amounts (Junghans et al, 2001).…”

Section: Discussionmentioning

confidence: 99%