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Aim: In this study, it was aimed to investigate the effect of coenzyme Q10 (CoQ10) on cisplatin-induced oxidative retinal damage in rats biochemically and histopathologically., Materials and Methods: Thirty male Wistar albino rats were divided into 3 groups randomly: untreated control (C group), only 2.5 mg/kg cisplatin daily administrated group for 2 weeks (CP group), 2.5 mg/kg cisplatin + 20 mg/kg orally CoQ10 daily administrated group for 2 weeks (CoQC group). At the end of experimental period, blood samples obtained before sacrification for the biochemical examination of serum malondialdehyde (MDA), total glutathione (tGSH), total oxidant system (TOS), total antioxidant systemic (TAS) levels and after eyes were removed for examined histopathology., Results: As a result of our study, severe histopathological damage was detected in the retinal tissue of the cisplatin group with serum malondialdehyde (MDA) and total oxidant system (TOS) levels were high and total glutathione (tGSH) and total antioxidant systemic (TAS) levels were low. However, it was observed that the histopathological damage associated with cisplatin was decreased in the retinal tissue of the CoQ10 group, which inhibited the increase in blood serum MDA/TOS levels and decrease in tGSH/TAS levels., Conclusion: The biochemical and histopathological results of our study were compatible with each other, so we concluded that the damage to the rat retinal tissue caused by cisplatin may be reversible with coenzyme.

Background: Cisplatin is a non-specific platinum-based (derivative) chemotherapeutic agent that causes an increase in free radicals activity in the liver. Antioxidant activity of taxifolin has been demonstrated previously, and it has been reported that taxifolin inhibits the hydroxyl, radical in experimental studies., Objectives: No studies were found in the current literature examining the protective effect of taxifolin on cisplatin-induced oxidative liver damage. We aimed to determine the protective effect of taxifolin on cisplatin-induced hepatotoxicity in an experimental study., Material and Methods: In total, 18 albino Wistar male rats were assigned into 3 groups: healthy controls (HC group), 5 mg/kg of cisplatin administered for 8 days (CIS group) and 50 mg/kg of taxifolin + 5 mg/kg of cisplatin administered for 8 days (TCG group). Malondialdehyde (MDA), total glutathione (tGSH), total oxidant (TOS), and total antioxidant (TAS) capacity levels were measured in the extracted liver tissue., Results: Liver tissue MDA and TOS levels were significantly higher in the CIS group. In contrast, tGSH and TAS levels were significantly lower in the CIS group, administered cisplatin alone (p < 0.001), compared to other groups. In the TCG group, administered cisplatin + taxifolin, MDA and TOS levels were significantly lower, whereas tGSH and TAS levels were significantly higher than in the CIS group (p < 0.001)., Conclusions: These results suggest that taxifolin may be useful in preventing cisplatin-related liver injury.

Aim: To investigate the effect of taxifolin on cisplatin-induced oxidative and proinflammatory optic nerve damage in rats., Methods: A total of 18 albino Wistar male rats were assigned into 3 groups, as follows; Group 1: Control group, Group 2: Only cisplatin administered group for 14 days (Cisplatin group), and Group 3: Taxifolin + cisplatin administered group for 14 days (CIS + TAX group). Serum malondialdehyde (MDA), total Glutathione (tGSH), Nuclear Factor-Kappa B (NF-ƘB), Total Oxidative Status (TOS) and Total Antioxidant Status (TAS) levels were collected from the left eyes of rats. Rats' right eyes were enucleated for histopathological evaluations of optic nerves., Results: NF-ƘB, MDA and TOS levels were statistically significantly higher ( p  < 0.001) in cisplatin group when compared to other 2 groups, the tGSH and TAS levels of which were statistically significantly lower ( p  < 0.001). Regarding these parameters, in cisplatin group NF-ƘB, MDA and TOS levels were statistically significantly increased with cisplatin administration and giving taxifolin concomitantly with cisplatin prevented this elevation. On the other hand, tGSH and TAS levels were statistically significantly decreased with cisplatin administration and routine simultaneous application of taxifolin with cisplatin prevented this decrease. In histopathological findings, haemorrhage was observed in the perineum of the injured optic nerves in the cisplatin treated group. And also edoema and degeneration in nerve fascicles in damaged optic nerves were seen in the cisplatin group. In the taxifolin treated group histopathological examinations were close to normal appearance, except mild edoema in nerve fascicles., Conclusion: Cisplatin causes oxidative stress on the rat optic nerves, and these changes lead to significant histopathological damage. Taxifolin, which we used to prevent oxidative damage to the optic nerves caused by cisplatin, has been emphasized as a powerful antioxidant agent in many previous scientific investigations. Concomitant administration of taxifolin may prevent these adverse effects of cisplatin, as well as histopathological damage. Further studies are needed to fully determine the effects of cisplatin and taxifolin on the eye.

Background: Cisplatin, used in cancer treatment, has toxic and apoptotic effects on the peripheral nervous system. Rutin, also known as vitamin P, has antioxidant and antiapoptotic activity., Objectives: The purpose of this study was to investigate the biochemical and histopathologic efficacy of rutin on neurotoxic and apoptotic effects caused by cisplatin in the peripheral nervous system., Material and Methods: Twenty-four albino Wistar male rats were divided into the following 4 groups: control group (CG), only cisplatin-injected group (CIS), cisplatin and rutin 50 mg/kg (RG-50)-injected group, and cisplatin and rutin 100 mg/kg (RG-100)-injected group. Analyses were performed on sciatic nerve tissue of experimental animals. Analyses of malondialdehyde (MDA), total glutathione (tGSH), glutathione reductase (GSHRd), glutathione-s-transferase (GST), and superoxide dismutase (SOD) were performed. Caspase-3 expression in nerve tissue was also investigated. The analyzed groups were compared with CG., Results: Biochemical investigation shows that there is a statistically significant difference between CG and only CIS and RG-50. Control group and RG-100 were found to be similar. Cisplatin-induced changes were observed in histopathological analysis of the nerve tissue. The RG-100 and CG were found to be similar. The caspase-3 expression in the neural tissue was compared between groups. Control group and CIS were found to be different. Control group and RG-100 were found to be similar., Conclusions: Antioxidant and antiapoptotic effectiveness of rutin was detected against the toxic effects caused by cisplatin in the peripheral nerve tissue.

Aim: Lutein is one of the most common carotenoids defined in human plasma as having potent anti-oxidant effects. We aimed to determine the biochemical and histopathological effects of lutein on cisplatin-induced oxidative retinal injury in rats., Materials and Methods: Twenty-four rats were equally divided into four groups as healthy controls (HC group), only cisplatin (5 mg/kg) administered group (CIS group), Lutein (0.5 mg/kg) + cisplatin (5 mg/kg) administered group (LC group), and only Lutein (0.5 mg/kg) (LUT group) administered group. From the blood samples obtained, serum malondialdehyde (MDA), total glutathione (tGSH), interleukin 1 beta (IL-1β), and tumor necrosis factor alpha (TNF-α) levels were investigated. In histopathological analyses, the total retinal thickness, retinal pigment epithelium (RPE), photoreceptor layer (PL), outer nuclear layer (ONL), outer plexiform layer (OPL), inner nuclear layer (INL), inner plexiform layer (IPL), and ganglion cell layer (GCL) were evaluated., Results: MDA, IL-1β, and TNF-a levels were statistically significantly higher (p < 0.001) in CIS group compared with other three groups while tGSH levels were statistically significantly lower (p < 0.001). In subgroup analyses, there was no any statistically significant difference regarding all four parameters analyzed between HC, LC, and LUT groups. In histopathological analyses, cisplatin-induced retinal damage included atrophy and disorganization on outer segment, degeneration and detachment of RPE and PL from choroid, degeneration and edema of INL and IPL, total degeneration of GCL; while cisplatin-induced retinal damage was determined to be significantly prevented with 0.5 mg lutein treatment on histopathological evaluations., Conclusions: Lutein co-administration was highly effective in prevention of cisplatin-induced retinal damage due to the anti-oxidant and anti-inflammatory effects of lutein.

Objective: Cisplatin is an anticancer drug used for treating childhood solid tumors. Symptoms related to cisplatin-induced cardiovascular adverse effects may be mild or severe. Rutin (vitamin P1) has many properties, including as antioxidant, anticancer, antidiabetic, antimicrobial, antiulcer, and tissue renewal properties. Therefore, we aimed to biochemically, histopathologically, and immunohistochemically demonstrate the effect of rutin on cisplatin-induced cardiotoxicity in rats., Methods: The rats included in our study were divided into four groups: Healthy group (HE), 5-mg/kg cisplatin group (CP), 50 mg/kg rutin+5-mg/kg cisplatin (CR-50), 100-mg/kg rutin+5-mg/kg cisplatin (CR-100) group., Results: CP group administered cisplatin had significantly increased blood, serum, and cardiac tissue malondialdehyde (MDA), interleukin 1 beta (IL-1ß), tumor necrosis factor alpha (TNF-α), troponin I, creatine kinase (CK), and CK-MB levels compared to the HE group, whereas there was a significant decrease in the total glutathione (tGSH) levels. Rutin was observed to prevent the increase in MDA, IL-1ß, TNF-α, troponin I, CK, and CK-MB levels as well as prevent the decrease in tGSH levels more significantly when administered at a 100-mg/kg dose than at a 50-mg/kg dose. Histopathologically, cardiac necrosis, dilated/congested blood vessels, hemorrhage, polymorphonuclear leukocyte, edema, and cells with pyknotic nuclei were observed in the CP group. Rutin was shown to prevent cisplatin-induced cardiac damage more effectively when used at a100-mg/kg dose than at a 50-mg/kg dose., Conclusion: These results suggest that rutin is useful for preventing cisplatin-related cardiovascular damage.

Aim: To determine the role of rutin in prevention of cisplatin induced retinal and optic nerve injury in an experimental study., Materials and Methods: 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., Results: 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)., Conclusions: 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.

Background/aims: To investigate the importance of antioxidant activity in infertility caused by cisplatin in rats., Methods: Rats in cisplatin control (CG), Vitamin E + cisplatin (ECG), Vitamin C + cisplatin (CCG), Hippophae rhamnoides extract (HRE) + cisplatin (HRECG), and thiamine pyrophosphate (TPP) + cisplatin (TPPCG) groups were injected intraperitoneally (ip) with (100 mg/kg) Vitamin E, Vitamin C, HRE, and TPP, respectively. One hour later, ip cisplatin was administered (5 mg/kg), and then antioxidant medications were continued for 10 days. Cisplatin + Vitamin E (CEG-1), cisplatin + Vitamin C (CCG-1), cisplatin + HRE (CHREG-1), and cisplatin + TPP (TPPCG-1) rats received cisplatin (5 mg/kg, ip) and were kept for 10 days. At the end of that period, rats received antioxidant medications for 10 days. (n = 12, for each group). Six rats from each group were sacrificed. Ovaries were removed to measure malondialdehyde, total glutathione, glutathione S-transferase, and glutathione reductase levels. The remaining rats were kept in a suitable laboratory environment., Results: Cisplatin-induced oxidative stress was best prevented by HRE, Vitamin E, Vitamin C, and TPP, in that order. However, infertility caused by cisplatin was only prevented and treated by TPP., Conclusion: Oxidative stress is not a major component in the pathogenesis of cisplatin-associated infertility., (© 2015 S. Karger AG, Basel.)

Ototoxicity of cisplatin is one of the major dose-limiting side effects. Cisplatin-dependent ototoxicity is known to be associated with reactive oxygen species. Protective effect of taxifolin, being a flavanone found in onions, milk thistle, French maritime, and Douglas fir bark, against cisplatin-associated ototoxicity will be examined in this study. There are no studies in the literature examining the protective effect of taxifolin against cisplatin-induced ototoxicity. 50 mg/kg taxifolin was orally administered to TXC group rats (n-6), and distilled water was orally administered as a solvent to CG (n-6) and HG (n-6) groups. One hour later, 5 mg/kg cisplatin was administered intraperitoneally (i.p) to TXC and CG groups. This procedure was repeated once a day for 7 days. At the end of this period, all animals were sacrificed by high-dose anesthesia (50 mg/kg thiopental sodium) and biochemical and histopathological examinations were performed on the dissected cochlear tissue. Our biochemical test results showed that oxidant parameters were significantly increased whereas antioxidant parameters were significantly decreased in the cisplatin group (CG) compared to taxifolin (TXC) and healthy (HG) groups (p < 0.0001 for both parameters). Histopathological results showed that severe cochlear vestibular membrane degeneration, dilated conjunctival blood vessels, edema and destruction developed in the cisplatin group. However, no pathological findings were found in the taxifolin-treated group except for mild degeneration and edema. This information suggests that taxifolin may be useful in the treatment of cisplatinassociated oxidative cochlear damage. [ABSTRACT FROM AUTHOR]