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Aim To investigate the effects of resveratrol on oxidative stress and inflammation parameters and histological alterations in cisplatin-induced optic nerve damage in a mouse model. Material and method Thirty-six albino Wistar male rats were divided into three groups as control, 5 mg/kg cisplatin-administered (Cis) and 5 mg/kg cisplatin + 25 mg/kg resveratrol-administered (Cis + Res) animals. At the end of the experimental period, the rats were sacrificed with high-dose (50 mg/kg) thiopental sodium, and their optic nerves were dissected. Malondialdehyde (MDA), total glutathione (tGSH), total oxidant status (TOS), total antioxidant status (TAS), tumour necrosis factor alpha (TNF-α), nuclear factor kappa B (NF-KB) levels, and histopathological findings were assessed using the optic nerve tissues. Results In the Cis + Res group, the MDA, TOS, OSI, TNF-a and NFK-B levels were significantly lower and the tGSH and TAS levels were significantly higher compared with the Cis group (P = 0.001). In histological evaluations, there were dilated and congested blood vessels, destruction, oedema, degeneration, haemorrhage, and proliferating capillaries indicating the presence of inflammation and damage only in the Cis-administered group. However, in the Cis + Res group, the histological findings were very similar to the healthy controls. Conclusion Resveratrol is a promising neuroprotective agent for cisplatin-induced optic nerve toxicity with its anti-oxidant and anti-inflammatory effects. Further investigations are needed to evaluate the possible therapeutic effects on other optic nerve toxicities.

Aim: Glaucoma is an optic neuropathy causing progressive impairment of visual functions. We aimed to assess the alterations in thiol-disulfide homeostasis and serum ischemia modified albumin (IMA) levels, which are the determinants of antioxidant status, in patients with primary open-angle glaucoma (POAG). Material and Method: A total of 140 eyes from 70 patients with POAG and 174 eyes of 87 healthy, control cases were included in the study. All study participants underwent a complete ophthalmic evaluation. Alterations in serum thiol-disulfide homeostasis and IMA levels were measured in all participants. Results: IMA levels were significantly higher in glaucoma group (p:0.001). Native thiol, Total thiol and Native/Total thiol ratio were significantly decreased while Disulfide, Disulfide/Native thiol, and Disulfide/Total thiol ratios were significantly higher in glaucoma group (p:0.001). There was no significant difference regarding central corneal thickness (CCT), iridocorneal angle, albumin, IMA and adjusted IMA levels in patients with different stages of glaucoma. In correlation analysis, there was a negative correlation between Native thiol, Total thiol and Native/Total thiol ratio and disease period, number of daily drops required and stage of the disease in glaucoma patients. There was also a positive correlation between Disulfide, Disulfide/Native thiol and Disulfide/Total thiol levels and the disease activity. Conclusion: In patients with POAG, thiol-disulfide homeostasis is disturbed in the favor of pro-oxidant molecules and IMA levels are increased, indicating the presence of augmented oxidative stress. In that aspect, systemic and local anti-oxidant treatments may be new targets in glaucoma treatment. Larger, prospective studies about the role of anti-oxidants in prevention and treatment of POAG are warranted.

Ethambutol and isoniazid are two major effective first line agents in tuberculosis treatment having some visual adverse effects. We aimed to determine the protective effects of lutein on oxidative optic neuropathy induced by ethambutol and isoniazid in an experimental model.Totally 24 albino Wistar male rats were assigned into 4 groups, with 6 rats in each group as follows: healthy controls (HC group), 50 mg/kg ethambutol +50 mg/kg isoniazid administered group (EI), 0.5 mg/kg lutein +50 mg/kg ethambutol +50 mg/kg isoniazid administered group (LEI-05) and only Lutein (0.5 mg/kg) (LUT group) administered group. From the blood samples and tissues obtained from the rats, Malondialdehyde (MDA), total glutathione (GSH), interleukin 1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) levels were studied. Histopathological evaluations were performed at the end of the study.Serum and tissue IL-1β, TNF-α and MDA levels were the highest in EI group which were significantly lower in lutein administered group. On the other hand, serum and tissue total GSH levels were the lowest in EI group which were significantly higher in Lutein administered group. In histopathological evaluations, there were significant differences between EI group and all other three groups with edema and hemorrhage in connective tissue covering optic nerve, dilated and congested capillary, decrease in astrocytes and oligodendrocytes.Isoniazid and ethambutol induced toxic optic neuropathy although not common, may have some potential devastating effects on vision. Lutein is determined as an effective agent in prevention of isoniazid and ethambutol induced toxic optic neuropathy.

To determine the role of rutin in prevention of cisplatin induced retinal and optic nerve injury in an experimental study.Totally 18 albino Wistar male rats were assigned into three groups, as follows: healthy controls (HC group), only cisplatin administered group for 14 days (CIS group), and rutin + cisplatin administered group for 14 days (RC group). Blood samples were obtained from animals just before the scarification. Serum malondialdehyde (MDA), myeloperoxidase (MPO), total glutathione (tGSH), superoxide dismutase (SOD), interleukin 1 beta (IL-1β) and tumour necrosis factor alpha (TNF-α) levels were investigated. The eyes were enucleated for histopathological evaluations of retina and optic nerve.MDA, MPO, IL-1β and TNF-α levels were statistically significantly higher (p 0.001) in CIS group compared with other two groups while tGSH and SOD levels were statistically significantly lower (p 0.001). Regarding these parameters, in CIS group MDA, MPO, IL1β and TNF-α levels were statistically significantly increased with cisplatin administration and giving rutin concomitantly with cisplatin prevented this increase. On the other hand, tGSH and SOD levels were statistically significantly decreased with cisplatin administration and giving rutin concomitantly with cisplatin prevented this decrease. In qualitative analyses of histopathological findings of retina and optic nerve; the results of RC group were similar with the results of healthy controls; but there was statistically significant differences between CIS group and other two groups (p 0.001).Concomitant rutin administration may prevent the detrimental effects of cisplatin on lipid peroxidation, oxidative stress and inflammation markers and may also avert the histopathological damage on retina and optic nerve. Further studies are warranted to determine the effects of cisplatin and rutin on eye.