The preventive effect of exogenous adenosine triphosphate on methanol-induced cardiotoxicity in rats

Exposure to methanol can cause serious consequences such as permanent visual disturbances and death. The heart tissue is highly vulnerable to ATP deficiency. Our study aimed to investigate whether exogenous ATP administration may alleviate methanol-induced ATP deficiency and subsequent oxidative damage in rat heart tissue. A total of 30 rats were divided into equal five groups; Healthy Group (HG), Methotrexate (MXG), Methanol (MeOH), Methotrexate+Methanol (MXM), and Methotrexate+Methanol+ATP (MMA) groups. We inhibited tetrahydrofolate synthesis by methotrexate to induce methanol toxicity. Methotrexate was administered to MXG, MXM, and MMA group animals for seven days with a catheter directly to the stomach at a 0,3 mg/kg dose per day. At the end of this period, % 20 methanol at a dose of 3 g/kg was administered to MeOH, MMA and MXM group animals. Immediately after methanol application, MMA group animals were injected with ATP at a 4 mg/kg dose intraperitoneally. Blood samples and heart tissues were used for biochemical analysis and histopathological examination. Co-exposure to methanol and methotrexate substantially exacerbated cardiac damage, indicating the potent cardiotoxic effects of methanol. However, the administration of exogenous ATP to MMA group animals brought biochemical oxidative damage parameters and histopathological findings closer to HG

The role of antioxidant activity in the prevention and treatment of infertility caused by cisplatin in rats

Kurt, Nezahat/0000-0002-1685-5332; AKSOY, Ayse Nur/0000-0002-3793-9797; AKSOY, Mehmet/0000-0003-0867-8660WOS: 000350267200009PubMed: 25632879Background/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. (C) 2015 S. Karger AG, Base

Effect of taxifolin on acrylamide-induced oxidative and proinflammatory lung injury in rats: Biochemical and histopathological studies

Purpose: To examine the probable beneficial effects of taxifolin against acrylamide damage in lung tissue.Methods: 18 male albino Wistar rats were divided into healthy (HG), acrylamide (AG) and taxifolin + acrylamide (TAG) groups. Once a day for 30 days, acrylamide was orally administered to the AG group (50 mg/kg), while ACL (50 mg/kg) and TAX (20 mg/kg) were orally administered to TAG group. Protein concentration, malondialdehyde (MDA), and total glutathione (tGSH) levels as well as oxidant and antioxidant molecules concentrations of the rat lung tissues were measured. In addition, degree of mononuclear (MN) cell infiltration and bronchial-associated lymphoid tissue (BALT) hyperplasia was evaluated by the degree of hyperplasia (absent, mild, moderate, severe). The histopathological andbiochemical data the groups were compared.Results: When compared in terms of MDA levels, it was found that the AG group had high MDA levels, and the TAG group had low MDA levels. (p < 0.001). TAG group was found to have a higher tGSH level than the AG group (p < 0.001). Compared to the AG group, lower TOS and higher TAS levels were obtained in the TAG group (p < 0.001). In addition, when TOS levels of TAG and HG groups were compared, the TOS levels between the two groups were statistically insignificant (p = 0.213). It has been observed that TAX administration prevents the increase in NF-ƘB level. When the NF-ƘB levels of the AG and TAG groups were compared with each other, there was a statistically significant difference (p = 0.001). In the AG group, severe MN cell hyperplasia and BALT hyperplasia were observed histopathologically. It was determined that these findings were alleviated in the TAG group. A histopathologically significant difference was found between AG and TAG groups (p < 0.05).Conclusion: Taxifolin has beneficial effects against lung injury caused by acrylamide, a healthdamaging environmental factor. Regular use of taxifolin can be recommended, especially in people who are known to have intense contact with acrylamide. There is a need for research studies on this subject

Effect of taxifolin on methotrexate-induced oxidative and inflammatory oral mucositis in rats: biochemical and histopathological evaluation

The role of oxidative stress, as well as inflammation in the pathogenesis of methotrexate (MTX)-induced oral mucositis, is a known fact. The anti-inflammatory, antitumor, antimicrobial, and antioxidant properties of taxifolin—the effect we tested against MTX-induced oral mucosal damage—are well known. Objective: Evaluating biochemically and histopathologically the effects of taxifolin on methotrexate-induced oral mucosal damage in rats. Methodology: In the taxifolin+MTX (TMTX) group, 50 mg/kg taxifolin was orally administered to rats by gavage. In the MTX and healthy (HG) groups, normal saline was applied to rats as solvent by the same method. One hour after administration of taxifolin and solvent, 5 mg/kg MTX was orally administered to rats in the MTX and TMTX groups. Taxifolin and methotrexate were administered once a day for 30 days. Macroscopic, biochemical, and histopathological evaluations were performed on the inner cheek and tongue tissues of rats. These parts were removed after rats were killed with a high-dose anesthesia. Results: Taxifolin with MTX prevented the increase in oxidant and pro-inflammatory parameters, such as malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), interleukin 6 (IL-6), on the inner cheek and tongue tissues of rats. Moreover, taxifolin antagonized the decrease in total glutathione (tGSH). Taxifolin decreased MTX-induced histopathological damage. Conclusion: These findings suggest that taxifolin may be useful to treat MTX-associated oral mucositis

The effects of metyrosine on ischemia-reperfusion-induced oxidative ovarian injury in rats: Biochemical and histopathological assessment

Abstract The aim of this study is to investigate the effect of metyrosine on ischemia-reperfusion (I/R) induced ovarian injury in rats in terms of biochemistry and histopathology. Rats were divided into: ovarian I/R (OIR), ovarian I/R+50 mg/kg metyrosine (OIRM) and sham (SG) operations. OIRM group received 50 mg/kg metyrosine one hour before the application of the anesthetic agent, OIR and SG group rats received equal amount of distilled water to be used as a solvent orally through cannula. Following the application of the anesthetic agent, ovaries of OIRM and OIR group rats were subjected to ischemia and reperfusion, each of which took two hours. This biochemical experiment findings revealed high levels of malondialdehyde (MDA) and cyclo-oxygenase-2 (COX-2) and low levels of total glutathione (tGSH), superoxide dismutase (SOD) and cyclo-oxygenase-1 (COX-1) in the ovarian tissue of OIR group, with significant histopathological injury. In metyrosine group, MDA and COX-2 levels were lower than the OIR group whereas tGSH, SOD and COX-1 levels were higher, with slighter histopathological injury. Our experimental findings indicate that metyrosine inhibits oxidative and pro-inflammatory damage associated with ovarian I/R in rats. These findings suggest that metyrosine could be useful in the treatment of ovarian injury associated with I/R

The preventive effect of exogenous adenosine triphosphate on methanol-induced cardiotoxicity in rats

Abstract Exposure to methanol can cause serious consequences such as permanent visual disturbances and death. The heart tissue is highly vulnerable to ATP deficiency. Our study aimed to investigate whether exogenous ATP administration may alleviate methanol-induced ATP deficiency and subsequent oxidative damage in rat heart tissue. A total of 30 rats were divided into equal five groups; Healthy Group (HG), Methotrexate (MXG), Methanol (MeOH), Methotrexate+Methanol (MXM), and Methotrexate+Methanol+ATP (MMA) groups. We inhibited tetrahydrofolate synthesis by methotrexate to induce methanol toxicity. Methotrexate was administered to MXG, MXM, and MMA group animals for seven days with a catheter directly to the stomach at a 0,3 mg/kg dose per day. At the end of this period, % 20 methanol at a dose of 3 g/kg was administered to MeOH, MMA and MXM group animals. Immediately after methanol application, MMA group animals were injected with ATP at a 4 mg/kg dose intraperitoneally. Blood samples and heart tissues were used for biochemical analysis and histopathological examination. Co-exposure to methanol and methotrexate substantially exacerbated cardiac damage, indicating the potent cardiotoxic effects of methanol. However, the administration of exogenous ATP to MMA group animals brought biochemical oxidative damage parameters and histopathological findings closer to HG

The Effect of Thiamine and Thiamine Pyrophosphate on Oxidative Liver Damage Induced in Rats with Cisplatin

The aim of this study was to investigate the effect of thiamine and thiamine pyrophosphate (TPP) on oxidative stress induced with cisplatin in liver tissue. Rats were divided into four groups; thiamine group (TG), TPP + cisplatin group (TPG), healthy animal group (HG), and cisplatin only group (CG). Oxidant and antioxidant parameters in liver tissue and AST, ALT, and LDH levels in rat sera were measured in all groups. Malondialdehyde levels in the CG, TG, TPG, and HG groups were 11 ± 1.4, 9 ± 0.5, 3 ± 0.5, and 2.2 ± 0.48 mol/g protein, respectively. Total glutathione levels were 2 ± 0.7, 2.8 ± 0.4, 7 ± 0.8, and 9 ± 0.6 nmol/g protein, respectively. Levels of 8-OH/Gua, a product of DNA damage, were 2.7 ± 0.4 pmol/L, 2.5 ± 0.5, 1.1 ± 0.3, and 0.9 ± 0.3 pmol/L, respectively. A statistically significant difference was determined in oxidant/antioxidant parameters and AST, ALT, and LDH levels between the TPG and CG groups ( < 0.05). No significant difference was determined between the TG and CG groups ( > 0.05). In conclusion, cisplatin causes oxidative damage in liver tissue. TPP seems to have a preventive effect on oxidative stress in the liver caused by cisplatin

The Effect of Anakinra on Acrylamide-induced Peripheral Neuropathy and Neuropathic Pain in Rats

Acrylamide is a neurotoxic compound. Moreover, anakinra is an interleukin-1 (IL-1) receptor antagonist used in rheumatoid arthritis treatment. This study investigated the effect of anakinra on acrylamide-related neuropathy and neuropathic pain. Acrylamide exposure caused a significant decrease in the pain threshold; an increase in malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β) levels; and a decrease in total glutathione (tGSH) values in the sciatic nerve. This indicates hyperalgesia presence, oxidative stress, and peripheral nerve tissue inflammation. Anakinra treatment significantly reduced the MDA, IL-1β, and TNF-α levels, and increased the pain threshold and mean tGSH values. The analgesic effect of anakinra was 67.9% at the first hour, increasing to 74.9% and 76.7% at the second and third hours, respectively. The group receiving acrylamide exhibited histopathological changes (e.g., swollen and degenerated axons, hypertrophic and hyperplasic Schwann cells, and congested vessels). The use of anakinra significantly improved these morphological changes. Anakinra is concluded to reduce neuropathic pain and prevent neurotoxic effect of acrylamide on peripheral nerves due to its analgesic, antioxidant, and anti-inflammatory properties

The Protective Effect of Thiamine Pryophosphate Against Sugar-Induced Retinal Neovascularisation in Rats

Cetin, Nihal/0000-0003-3233-8009;WOS: 000476915300003PubMed: 31165688The aim of this study was to investigate the effect of thiamine pyrophosphate (TPP), administered via sugar water, on retinal neovascularisation in rats. Animals were assigned to three groups, namely the TPP sugar-water group (TPSWG, n = 12), the control group (CG, n = 12) and the healthy group (HG, n = 12). the TPSWG was injected intraperitoneally with TPP once a day for 6 months. CG and HG rats were given distilled water in the same way. TPSWG and CG rats were left free to access an additional 0.292 mmol/ml of sugar water for 6 months. the fasting blood glucose (FBG) levels of the animals were measured monthly. After 6 months, biochemical, gene expression and histopathologic analyses were carried out in the retinal tissues removed from the animals after they were killed. the measured FBG levels were 6.96 +/- 0.09 mmol/ml (p < 0.0001 vs. HG), 6.95 +/- 0.06 mmol/ml (p < 0.0001 vs. HG) and 3.94 +/- 0.10 mmol/ml in the CG, TPSWG and HG groups, respectively. the malondialdehyde (MDA) levels were found to be 2.82 +/- 0.23 (p < 0.0001 vs. HG), 1.40 +/- 0.32 (p < 0.0001 vs. HG) and 1.66 +/- 0.17 in the CG, TPSWG and HG, respectively. Interleukin 1 beta (IL-1 beta) gene expression was increased (3.78 +/- 0.29, p < 0.0001) and total glutathione (tGSH) was decreased (1.32 +/- 0.25, p < 0.0001) in the retinal tissue of CG compared with TPSWG (1.92 +/- 0.29 and 3.18 +/- 0.46, respectively). Increased vascularisation and oedema were observed in the retinal tissue of CG, while the retinal tissues of TPSWG and HG rats had a normal histopathological appearance. A carbohydrate-rich diet may lead to pathological changes in the retina even in nondiabetics, but this may be overcome by TPP administration

Effect of Thiamine Pyrophosphate on Oxidative Damage to the Oropharyngeal, Nasal and Cochlear Tissues Induced by Doxorubicin in Guinea Pigs

Malkoc, Ismail/0000-0002-9221-510XWOS: 000406050300010Doxorubicin (DOX) inhibits the enzyme tyaminpyrophosphokinase (TPK). Hence the synthesis of thiamine pyrophosphate (TPP) which is the active metabolite of thiamine stops. This leads to oxidative damage. in the literature, no studies on the protective effect of TPP against doxorubicin-induced oropharyngeal, nose and cochlear oxidative damage were found. in this study was investigated whether DOX produces oxidative stress in the oropharyngeal, nose and cochlea of animals and it examines the protective effect of TPP against DOX toxicity on these tissues. Guinea pig experimental animals were divided into groups as the controls. One group was given DOX, another group was given TPP + doxorubicin (TDOX) and the final group was the healthy group (HG). the TDOX group (n = 6) received an intraperitoneal (ip) injection of 25 mg/kg TPP. the DOX (n = 6) and HG (n = 6) animals were given distilled water in the same way. TDOX and DOX animals were administered ip 5 mg/kg DOX one hour after the administration of TPP and distilled water once a day for seven days. At the end of this period, animals were sacrified with a high dose of anesthesia and the levels of malondialdehyde (MDA), myeloperoxidase (MPO), nitric oxide (NO), total glutathione (tGSH) and glutathione reductase (GSHRd) were determined in the removed oropharyngeal, nasal, and cochlear tissues. in addition, the TNF-alpha gene expression was measured. DOX was demonstrated to significantly increase the levels of MDA, MPO and NO and to reduce the levels of tGSH and GSHRd in the oropharyngeal, nasal and cochlear tissues of animals. TPP prevented the increase of the levels of MDA, MPO, NO and TNF-alpha with doxorubicin. TPP supressed the oxidative stress induced by DOXin the oropharyngeal, nasal and cochlear tissues. It can be suggested that TPP can be used against DOX toxicit