The effects of lutein on cisplatin-induced retinal injury: an experimental study

Karakurt, Yücel; Uçak, Turgay; Tasli, NurdanGamze; Ahiskali, Ibrahim; Şipal, Sare; Kurt, Nezahat; Süleyman, Halis

doi:10.1080/15569527.2018.1482494

Cited by 15 publications

(10 citation statements)

References 27 publications

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“…Our histopathological findings of increased FOR and proinflammatory mediator production conforms to those reported elsewhere (28,29). In addition, a study by Karakurt et al, have also demonstrated the antioxidant activity of lutein and its inhibitory effect on proinflammatory cytokine production (30).…”

Section: Discussionsupporting

confidence: 92%

The Effect of Lutein on Ischemia-reperfusion-induced Vasculitic Neuropathic Pain and Neuropathy in Rats

Yuceli

Yazıcı

Mammadov

et al. 2021

In Vivo

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Background/Aim: Neuropathic pain and neuropathy is commonly seen after ischemia-reperfusion injuries. Our aim was to evaluate the effect of lutein on ischemia-reperfusion (I/R)induced vasculitic neuropathic pain and neuropathy in rats. Materials and Methods: An hour before anesthesia, 6 Albino Wistar male rats with I/R were orally administered with 1 mg/kg lutein (LIR group). Two groups of 6 such rats who underwent surgery were provided with 0.5 ml distilled water (as solvent) either via oral administration (SIR group) or by gavage (sham group or SG). One hour following the administration, the later femoral arteries of the LIR and SIR rats were closed using a sterile silk thread and ischemia was induced in the sciatic nerve for 4 h, followed by reperfusion for 24 h. The femoral artery of the SG group was not closed with suture. Next, 1 mg/kg lutein was re-administered only to the LIR group for 1 h, followed by measurement of the paw pain thresholds by the Basile Algesimeter. The levels of malondialdehyde (MDA), total glutathione (tGSH), nuclear factor-kB (NF-ĸB), and tumor necrosis factor-alpha (TNF-α) in the sciatic nerve tissues were measured, and the tissues were histopathologically examined. Results: We found that the MDA, NF-ĸB, and TNF-α levels were higher and the tGSH level was lower in the SIR group relative to those in the LIR group, and the differences were statistically significant. Significant histopathological damage was noted in the SIR group, whereas the LIR group demonstrated protection from oxidative damage. Conclusion: Lutein is potentially useful in the treatment of I/R-related neuropathy and neuropathic pain.Ischemia-reperfusion (I/R) injury is a complex pathological process that begins with a decrease in the tissue oxygen levels, followed by the production of free oxygen radicals, resulting in an inflammatory response (1). The I/R event in the vascular and nervous systems have been documented with an increasing ischemic and vasculitic neuropathic pain that clinically resembles the complex regional pain syndrome (2). In isolated vasculitis, a form of vasculitic neuropathy of the peripheral nervous system, medium-and small-size vessels in peripheral nerves are usually affected (3). The incidence of vasculitic neuropathies is greater in the lower extremities and causes severe pain (4). Some reports assert that neuropathy may be the first or even the only indicator of vasculitis ( 5).An I/R event is also known to induce significant damages to the nerve cells as well as to the internal organs (6). Reportedly, the I/R process induces microvascular changes, which lead to structural and functional disorders of nerve tissues (7). The pathophysiology of I/R injury consists of a complex event that involves the obstruction of the capillaries, immune cell activation, free oxygen radical (FOR) production, lipid peroxidation (LPO), and increased antioxidant expenditure (8,9). The together, these data suggest that drugs with antioxidant and anti-inflammatory properties may be useful in the treatment of vasc...

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Section: Discussionsupporting

confidence: 92%

The Effect of Lutein on Ischemia-reperfusion-induced Vasculitic Neuropathic Pain and Neuropathy in Rats

Yuceli

Yazıcı

Mammadov

et al. 2021

In Vivo

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“…Previous studies on several different tissue types have shown that oxidative stress causes increased MDA levels and decreased tGSH levels, 12,34–36 and the same was found in the MTX group in this study. However, CoQ10 was found to reverse these effects almost to the level of the control group, suggesting that MTX produces oxidative stress in ovarian tissues and that CoQ10 can ameliorate this damage.…”

Section: Discussionsupporting

confidence: 87%

Protective effect of Coenzyme Q10 on oxidative ovarian and uterine damage induced by methotrexate in rats

Kiremitli

Akselim

et al. 2021

Hum Exp Toxicol

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Methotrexate (MTX) has toxic effects on the uterus and ovaries via oxidative stress. Coenzyme Q10 (CoQ10) is an important component in electron transport in the mitochondria and an antioxidant in cellular metabolism through the inhibition of lipid peroxidation. The aim of this study was to investigate the preventive effects of CoQ10 on MTX-induced utero-ovarian damage and oxidative stress in rats. In this experimental study, 30 albino Wistar female rats were divided randomly into three groups. Once a day for a month, 10 mg/kg of CoQ10 was orally administered to the rats in the MTX+CoQ10 group, while the same volume of olive oil was administered orally to the other two groups. One hour thereafter, 20 mg/kg of MTX was injected intraperitoneally into the rats in the MTX and MTX+CoQ10 groups; the remaining group was the control. At the end of the month, biochemical and histopathologic examinations were performed on the extracted uteri and ovaries. In the uterine ovarian tissues of the animals in the MTX group, there was an increase in oxidative stress mediators and a decrease in antioxidant and anti-inflammatory mediators, but these trends were reversed in the MTX+CoQ10 group, demonstrating the antioxidant effects of CoQ10. MTX leads to oxidative stress-related ovarian and uterine injury, and CoQ10 may be useful for protecting ovarian and uterine tissue from such injury.

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“…Recently, cisplatin has been reported to elevate the MDA level in blood serum. In addition, it has been noted that increase in MDA levels in blood serum with cisplatin causes damages in tissue as well [4]. Cisplatin has been reported to perform such effects by increasing the ROS production and in addition to an increase in the production of superoxide anion, hydrogen peroxide and hydroxyl radicals [28].…”

Section: Il-1b and Tnf-a Levels In Bladder Tissuementioning

confidence: 99%

“…It has also been found that oxidative stress is responsible for cisplatin neurotoxicity [3]. Karakurt et al [4] have shown that animals with high levels of malondialdehyde (MDA), interleukin 1 beta (IL-1b) and tumor necrosis factor alpha (TNF-a) and low level of total glutathione (tGSH) in the blood serum of the cisplatin group develop severe damage in the retina histopathologically. In recent studies, cisplatin-induced neuropathic pain has been associated with oxidative stress [5].…”

Section: Introductionmentioning

confidence: 99%

Effect of rutin on oxidative and proinflammatory damage induced by cisplatin in blood serum, ureter, bladder and urethra in rats

Hirik

Bozkurt

Keskin

et al. 2020

Biotechnology & Biotechnological Equipment

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Rutin (Vitamin P1) is an antioxidant and anti-inflammatory flavonoid. This study examined the effect of rutin on the potential of cisplatin to cause oxidative and proinflammatory damage in blood serum, ureter, bladder and urethra in rats. Animals were divided into four groups: (i) healthy (HG), (ii) 50 mg/kg of rutin þ 5 mg/kg of cisplatin (C þ R50), (iii) 100 mg/kg of rutin þ 5 mg/kg of cisplatin (C þ R100) and (iv) only cisplatin (CG). Rutin and distilled water were applied once a day for eight days. Cisplatin was injected intraperitoneally at a dose of 5 mg/kg for eight days, once every two days. Finally, animals were sacrificed by high-dose anesthesia after blood samples were taken. Ureter, bladder and urethra tissues were removed and malondialdehyde (MDA), myeloperoxidase (MPO), total glutathione (tGSH), superoxide dismutase (SOD) interleukin beta (IL-1b) and tumor necrosis factor alpha (TNF-a) levels were measured. The results showed that the levels of MDA, MPO, IL-1b and TNF-a in the blood serum of the CG group increased significantly (p < 0.0001) and the tGSH and SOD levels decreased compared to the HG. Rutin administration reversed the effect as seen in C þ R50 and C þ R100 groups. However, there was no statistically significant difference in the levels of MDA, MPO, tGSH, SOD, IL-1b and TNF-a in ureter, bladder and urethra tissue (p > 0.05).This suggests that cisplatin produces oxidative stress in the blood serum but not in the ureter, bladder and urethra tissues. It was observed that rutin prevented the cisplatin-related oxidative and proinflammatory damage in the blood serum.

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The effects of lutein on cisplatin-induced retinal injury: an experimental study

Abstract: Lutein co-administration was highly effective in prevention of cisplatin-induced retinal damage due to the anti-oxidant and anti-inflammatory effects of lutein.

Cited by 15 publications

References 27 publications

The Effect of Lutein on Ischemia-reperfusion-induced Vasculitic Neuropathic Pain and Neuropathy in Rats

The Effect of Lutein on Ischemia-reperfusion-induced Vasculitic Neuropathic Pain and Neuropathy in Rats

Protective effect of Coenzyme Q10 on oxidative ovarian and uterine damage induced by methotrexate in rats

Effect of rutin on oxidative and proinflammatory damage induced by cisplatin in blood serum, ureter, bladder and urethra in rats

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