Lipid peroxidation and antioxidant enzymatic systems in rat retina as a function of age

Castorina, C.; Campisi, A.; Giacomo, Claudia Di; Sorrenti, Valeria; Russo, Alessandra; Vanella, A.

doi:10.1007/bf00968789

Cited by 56 publications

(21 citation statements)

References 42 publications

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“…The retina is especially susceptible to oxidative stress because of its high consumption of oxygen, its high proportion of polyunsaturated fatty acids and its exposure to light. Among others, GSH and antioxidant enzymes such as SOD, catalase and GSH peroxidase provide a powerful antioxidant defense in the retina [32,33,34]. …”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Crocin against Oxidative Stress Induced by Ischemia/Reperfusion Injury in Rat Retina

Chen

Yang

2015

Ophthalmic Res

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Aims: Crocin, a pharmacologically active component of Crocus sativus L. (saffron), has been reported to be useful in the treatment of oxidative stress injury. In the present study, we investigated the antioxidative effect of crocin and the change of the ERK signaling pathway on rat retina induced by ischemia/reperfusion (IR) injury. Methods: Crocin was pretreated 30 min before and once daily after retinal IR injury by intraperitoneal injection. The retinal morphological damage was observed by hematoxylin and eosin (HE) staining. The number of retinal ganglion cells (RGCs) was counted by Brn-3a immunofluorescence staining. The antiapoptotic effect of crocin was determined by detecting cleaved caspase-3 protein levels by means of Western blot and immunohistochemical analysis. Furthermore, retinas were also used for the determination of malondialdehyde (MDA) levels, glutathione (GSH) levels, total superoxide dismutase (T-SOD), and reactive oxygen species (ROS). The phosphorylated ERK (p-ERK) protein level was determined by Western blot and immunohistochemical analysis. Results: Our results showed that crocin treatment (50 mg/kg) significantly inhibited the decrease of retinal thickness through HE staining and protected RGCs from decreasing. Compared with the IR + vehicle group, crocin treatment significantly decreased cleaved caspase-3 and p-ERK protein expression by Western blot analysis and immunohistochemistry. Immunohistochemical staining for cleaved caspase-3 and p-ERK in the retinal sections showed positive cells were present in the RGC layer and inner nuclear layer after IR injury. Similarly, crocin (50 mg/kg) treatment also significantly increased the level of activity of GSH, enhanced the activity of T-SOD, and decreased the activity level of ROS and MDA after IR injury. Conclusions: These findings demonstrated that crocin treatment could notably protect the retina from damage induced by IR. It might be related to crocin antioxidant and antiapoptotic properties in the retina.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Crocin against Oxidative Stress Induced by Ischemia/Reperfusion Injury in Rat Retina

Chen

Yang

2015

Ophthalmic Res

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“…In addition to chaperone-mediated activity (37), HSPs combat oxidative stress by increasing levels of glutathione and modulating the redox status of cells (38). Decreasing levels of glutathione and associated proteins with age (39,40), coupled with constitutively decreased expression of these important homeostatic gene families in young A/J mice compared with BALB/c and B6 mice, could explain the accelerated ARD phenotype found in A/J mice. Pathologic changes seen in A/J RPE, characterized by cell swelling and buildup of undigested disc elements, have also been reported in albino and pigmented rats deprived of selenium (41,42), a critical cofactor for activation of antioxidant proteins such as GPX3.…”

Section: Pathway Analysis Highlights Inflammatory Priming Coupled Witmentioning

confidence: 99%

Inflammatory priming predisposes mice to age-related retinal degeneration

Mustafi¹,

Maeda²,

Kohno³

et al. 2012

J. Clin. Invest.

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Disruption of cellular processes affected by multiple genes and accumulation of numerous insults throughout life dictate the progression of age-related disorders, but their complex etiology is poorly understood. Postmitotic neurons, such as photoreceptor cells in the retina and epithelial cells in the adjacent retinal pigmented epithelium, are especially susceptible to cellular senescence, which contributes to age-related retinal degeneration (ARD). The multigenic and complex etiology of ARD in humans is reflected by the relative paucity of effective compounds for its early prevention and treatment. To understand the genetic differences that drive ARD pathogenesis, we studied A/J mice, which develop ARD more pronounced than that in other inbred mouse models. Although our investigation of consomic strains failed to identify a chromosome associated with the observed retinal deterioration, pathway analysis of RNA-Seq data from young mice prior to retinal pathological changes revealed that increased vulnerability to ARD in A/J mice was due to initially high levels of inflammatory factors and low levels of homeostatic neuroprotective factors. The genetic signatures of an uncompensated preinflammatory state and ARD progression identified here aid in understanding the susceptible genetic loci that underlie pathogenic mechanisms of age-associated disorders, including several human blinding diseases. IntroductionAge-related disorders arise from failure of tissue maintenance and repair pathways that are accelerated by certain inherited and acquired factors (1). Long-lived nondividing cells, such as neurons, have markedly reduced tolerance to damage (2), and thus exhibit the most pronounced age-related changes. Neuronal cells in the retina are an especially attractive model system to study this phenomenon, owing to their accessibility and wellunderstood physiology. Rod and cone photoreceptors are retinal neuronal cells that initiate visual perception, a function requiring a competent neighboring retinal pigmented epithelium (RPE) for their normal operation (3). In postmitotic cells such as these photoreceptor and RPE cells, cellular senescence can ensue when shed oxidized photoreceptor outer segments (POS) are inadequately phagocytosed and digested by the RPE. This results in accumulation of damaged proteins, formation of toxic metabolic byproducts, inflammatory cell invasion, and cell death. RPE cells are the most affected because, in addition to processing POS, they serve as the conduit between photoreceptors and the choroidal blood supply for metabolite exchange (4). Acquisition of senescence-associated pathology stimulates cells to secrete various factors that contribute to tissue dysfunction. Conversely, adequate clearance of such cells can delay the onset of age-related tissue pathology (5).Aging laboratory experimental animals are important models for studying age-related pathology, especially neurodegenerative disorders, which have been shown to be affected by their genetic backgrounds (6, 7). The A/J inbred mouse ...

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“…Aged rat retina showed decreased GSH-Px and catalase activities, which are related to increased lipid peroxidation with age 11 . In particular, RPE cells accumulate lipofuscin granules during life.…”

Section: Oxidative Stress and Amdmentioning

confidence: 97%

Nutritional Supplement Use and Age-Related Macular Degeneration

Lo¹,

Wong²

2012

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Lipid peroxidation and antioxidant enzymatic systems in rat retina as a function of age

Cited by 56 publications

References 42 publications

Neuroprotective Effects of Crocin against Oxidative Stress Induced by Ischemia/Reperfusion Injury in Rat Retina

Neuroprotective Effects of Crocin against Oxidative Stress Induced by Ischemia/Reperfusion Injury in Rat Retina

Inflammatory priming predisposes mice to age-related retinal degeneration

Nutritional Supplement Use and Age-Related Macular Degeneration

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