The aim of this study was to investigate the effects of Achillea millefolium extract in paclitaxel‐induced testicular toxicity in rats. The groups were designed as (1) control, (2) paclitaxel (8 mg/kg, intraperitoneally), (3) paclitaxel (8 mg/kg, intraperitoneally) + Achillea millefolium (200 mg/kg, orally for 14 consecutive days) and (4) paclitaxel (8 mg/kg, intraperitoneally) + Achillea millefolium (400 mg/kg, orally for 14 consecutive days). Serum levels of testosterone, luteinising hormone and follicle‐stimulating hormone, as well as total antioxidant capacity and total oxidant status were measured one day after receiving the last dose of Achillea millefolium extract. Testicular superoxide dismutase activity, malondialdehyde, tumour necrosis factor alpha and interleukin‐1β levels, the expressions of nuclear factor kappa B and caspase‐3 were evaluated. In addition, testicular sections were evaluated histopathologically and 8‐hydroxy‐2′‐deoxyguanosine was detected immunohistochemically. Achillea millefolium improved the levels of luteinising hormone, follicle‐stimulating hormone and testosterone, upregulated testicular antioxidant enzymes and downregulated inflammation. Furthermore, we observed that Achillea millefolium restored testicular histopathological structure and significantly suppressed oxidative DNA damage and apoptosis by reducing the expression of caspase‐3. Taken together, our results suggest that Achillea millefolium has protective effects against paclitaxel‐induced testicular toxicity and is a promising natural product with the potential to improve male fertility.

(1) Background: Various epidemiological studies suggest that oxidative stress and disrupted neuronal function are mechanistically linked to neurodegenerative diseases (NDs), including Parkinson’s disease (PD) and Alzheimer’s disease (AD). DNA damage, oxidative stress, lipid peroxidation, and eventually, cell death such as NDs can be induced by nitrosamine-related compounds, leading to neurodegeneration. A limited number of studies have reported that exposure to diethylnitrosamine (DEN), which is commonly found in processed/preserved foods, causes biochemical abnormalities in the brain. Artichoke leaves have been used in traditional medicine as a beneficial source of bioactive components such as hydroxycinnamic acids, cynarine, chlorogenic acid, and flavonoids (luteolin and apigenin). The aim of this study is to investigate the favorable effects of exogenous artichoke (Cynara scolymus) methanolic leaf extract supplementation in ameliorating DEN-induced deleterious effects in BALB/c mouse brains. (2) Methods: This study was designed to evaluate DEN (toxicity induction by 100 mg/kg) and artichoke (protective effects of 0.8 and 1.6 g/kg treatment) for 14 days. All groups underwent a locomotor activity test to evaluate motor activity. In brain tissue, oxidative stress indicators (TAC, TOS, and MDA), Klotho and PPARγ levels, and apoptotic markers (Bax, Bcl-2, and caspase-3) were measured. Brain slices were also examined histopathologically. (3) Results: Artichoke effectively ameliorated DEN-induced toxicity with increasing artichoke dose. Impaired motor function and elevated oxidative stress markers (decreasing MDA and TOS levels and increasing TAC level) induced by DEN intoxication were markedly restored by high-dose artichoke treatment. Artichoke significantly improved the levels of Klotho and PPARγ, which are neuroprotective factors, in mouse brain tissue exposed to DEN. In addition, caspase-3 and Bax levels were reduced, whereas the Bcl-2 level was elevated with artichoke treatment. Furthermore, recovery was confirmed by histopathological analysis. (4) Conclusions: Artichoke exerted neuroprotective effects against DEN-induced brain toxicity by mitigating oxidant parameters and exerting antioxidant and antiapoptotic effects. Further research is needed to fully identify the favorable impact of artichoke supplementation on all aspects of DEN brain intoxication.

Abstract. Aim of this work was to determine the effects of dietary intake vitamin E and Se on lipid peroxidation (LPO) as Thiobarbituric acid reactive substances (TBARS) and on the antioxidative defense mechanisms in heart tissues of rats treated with high doses of prednisolone. 250 adult male Wistar rats were randomly divided into 5 groups and fed with normal diet. Additionally groups 3, 4, and 5 received a daily supplement in their drinking water of 20 mg vitamin E, 0.3 mg Se, and a combination of vitamin E and Se (20 mg/ 0.3 mg), respectively, for 30 days. For 3 d subsequently, control group was treated with placebo, and remaining four groups were injected intramuscularly with 100 mg/kg prednisolone. After last administration of prednisolone, 10 rats from each group were killed at 4, 8, 12, 24, and 48 h and the activities of antioxidant enzymes and the levels of GSH and TBARS were measured. GSH-Px, CAT activities and GSH levels decreased starting from 4th hour to 48% and 65% of control levels by 24th hour, respectively and it reincreased to control levels at 48th hour in the prednisolone group (p < 0.001, p < 0.001). In addition, prednisolone administration led 2-fold increase in heart TBARS levels at 24th hour (p < 0.001). E vitamins and Se inhibited the increase in heart TBARS and the decrease in antioxidative enzymes levels. Therefore, It is concluded that vitamin E and Se may have a preventive role in decreasing the increase of TBARS caused by prednisolone administration in our study.

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Background and Objective: Metamizole is a non-selective cyclooxygenase (COX) inhibitor NSAID with a strong analgesic and spasmolytic effects. It is the most common analgesic in the world. Thiamine pyrophosphate (TPP) protects the liver tissue against oxidative damage. The aim of our study was to analyze the effect of TPP against possible liver injury and dysfunction of metamizole in rats biochemically and histopathologically. Materials and Methods: The animals were grouped as healthy (HG), 500 mg kgG 1 metamizole (MT-500), 1000 mg kgG 1 metamizole (MT-1000), 25 mg kgG 1 TPP+500 mg kgG 1 metamizole (TMT-500), 25 mg kgG 1 TPP+1000 mg kgG 1 metamizole (TMT-1000) groups. The TMT-500 and TMT-1000 groups of animals were injected intraperitoneally (ip) at the dose of 25 mg kgG 1 of TPP. Distilled water as the solvent was injected ip to the HG, MT-500 and MT-100 groups. One hour after injecting TPP and distilled water, metamizole 500 and 1000 mg kgG 1 doses were administered orally to the TMT-500 and TMT-1000 groups. The TPP was administered once and metamizole twice a day for 14 days. The animals were euthanized with high-dose anesthesia. The liver tissues excised from the animals were analyzed biochemically and histopathologically. Results: In both doses metamizole significantly increased MDA, ALT and AST levels and decreased tGSH, SOD and CAT levels compared to the healthy group. TPP significantly prevented the decrease of tGSH, SOD and CAT levels and the increase of MDA, ALT and AST levels with metamizole. There was no statistical difference in all of the levels between the TMT-500 and TMT-1000 groups. The histopathological findings indicated TPP significantly suppressed the damage induced by metamizole. Conclusion: The metamizole was possible to cause moderate damage to liver tissue. Therefore, it was considered that the use of TTP to reduce liver toxicity could be clinically beneficial.

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Undesirable side effects that result from the random use of herbicides in developing countries are widespread. Imazamox is a widely used herbicide and has toxic effect on humans. Momordica charantia has been reported to possess many benefits and medicinal properties. Pycnogenol (PYC) is a natural plant extract from the bark of Pinus pinaster Aiton and has potent antioxidant activities. The aim of this study was to evaluate the protective effects of pycnogenol and momardica on induced imazamox toxicity effects on L929 fibroblast cell line. L929 fibroblast cells were cultured in the appropriate culture medium. Toxic concentration of imazamox 250 μM, were administered 30 min prior to momordica and pycnogenol (10−1–10−5 concentration) on L929 fibroblast cell line for 24 h. The cell viability assay was determined by using MTT test. TAC-TOS analysis were used to evaluate antioxidant and oxidant status. According to our study pycnogenol high dose showned protective effect whereas momordica low dose showned protective effect p < 0.05. In current study pycnogenol increased TAC capacity in high dose but in lower dose pycnogenol did not show any promise (p < 0.05). Momordica results showed correlation with MTT result. According to this analyse momordica only in low dose increased anti oxidant capacity and in addition, only in low dose TOS level were decreased (p > 0.05). In conclusion momordica and pycnogenol showed promise to reduced imazamox toxicity.