The aim of the present study was to investigate the therapeutic and protective effects of linalool against doxorubicin (DOX)-induced kidney injury. Forty-eight Wistar rats were divided into 8 groups as follows; Control, DOX [20 mg/kg, intraperitoneal (ip) single dose DOX], linalool (LIN50 and LIN100; 50 mg/kg and 100 mg/kg linalool via ip for 5 days, respectively), DOX + LIN50 and DOX + LIN100 (20 mg/kg single dose of DOX via ip on first day and 50 mg/kg and 100 mg/kg linalool via ip, respectively), LIN50 + DOX and LIN100 + DOX (50 mg/kg and 100 mg/kg linalool via ip for 5 days, respectively and 20 mg/kg single dose of DOX via ip on fifth day). Doxorubicin led to a significant increase in the level of malondialdehyde (MDA) in the kidney, whereas superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH) levels decreased remarkably when compared with control. On the other hand, LIN supplementation before and after DOX treatment led to a significant decrease in MDA and also increases in SOD, CAT and GSH levels. DOX caused significant increases in the levels of blood urea nitrogen (BUN) and creatinine (Cr) levels in the plasma, while LIN supplementation as a therapeutic and preventive agent led to significant decreases in BUN and Cr levels. The current study demonstrated that LIN supplementation after or before DOX treatment can led to therapeutic and preventive effects against DOX-induced renal damage.

Breast cancer is the most common cancer in women ın the world. Many anticancer drugs are currently used clinically have been isolated from plant species or are based on such substances. Linalool is aromatic compounds from the monoterpene group. It is the main constituents of essential oils and show antiproliferative, antioxidant, and antiseptic properties. The aim of this study was to investigate the antiproliferativeand apoptotic, effects of linalool in MCF-7 and MDA-MB-231 human breast cancer cells. MCF-7 and MDA-MB-231 human breast cancer cells were treated with different concentrations of linalool (100, 200, 400, 600, 800, 1000 µM) at 24 h and 48 h. MTT assay for cell proliferation and Annexin V assay for apoptosis was done. The morphology of breast cancer cells was investigated by lıght mıcroscope and scanning electron microscope (SEM). The study show that linalool significantly induced apoptosis in all groups as dose and time-dependent (p < .05). Linalool has apoptotic and antiproliferative properties in a concentration and time-dependent manner in breast cancer cells. The cytotoxic effects of linalool on MCF-7 and MDA-MB-231 human breast cancer cells was found to be associated with apoptotic cell death. Linalool was more effective on MCF-7 human breast cancer cells in smaller amounts. Graphical Abstract

We investigated the effects of quercetin on cisplatin induced testicular toxicity using histopathological, immunohistochemical and biochemical methods. We used four groups of Wistar albino male: control, quercetin, cisplatin, cisplatin + quercetin. We measured tissue malondialdehyde (MDA) and catalase (CAT) biochemically. We assessed apoptosis as indicated by P63 immunoreactivity. Testis tissues of the control group exhibited normal histology. In the cisplatin group, the diameter of the seminiferous tubule and thickness of the germinal epithelium were decreased compared to the control group. In the cisplatin group, degeneration of the germinal epithelium, cell separation from the basal membrane, giant cell formation, cell loss, atrophy and vacuolization were observed in the seminiferous tubule. We found hyalinization around the seminiferous tubule, intertubule hyalinization and perivascular fibrosis. In the cisplatin + quercetin group, we found that quercetin decreased atrophy, giant cell formation and vacuolization significantly. We found that quercetin exhibited ameliorative effects following cisplatin induced testicular damage.

Excitotoxicity caused by excessive concentration of the excitatory neurotransmitter glutamate causes neuronal cell death and promotes neurodegenerative disorders. The neuroexcitant neurotoxin kainic acid (KA) induces excitotoxicity, leading to neuronal death via oxidative stress and inflammation, and its experimental use is widespread. This study was designed to determine the protective effect of Troxerutin (TXR) and its relationship with Galectin-3 (Gal-3) in experimental excitotoxicity with neuroinflammation and oxidative stress. Fifty male Wistar rats were divided into five groups ( n = 10): Control group rats received intraperitoneal (ip) normal saline for 6 days. Sham group rats received a single dose of intracerebroventricular (icv) normal saline on the first day. KA group rats were treated with a single dose of KA; icv-0.5 μg/μl). TXR group rats treated with TXR for 6 days: ip-100 mg/kg) and KA + TXR group rats treated with KA (single dose) and TXR (6 days). It was observed that malondialdehyde (MDA) and interleukin-1β (IL-1β) levels increased and reduced glutathione (GSH) levels decreased in the cerebral cortex of rats with KA neurotoxicity. TXR treatment caused a significant improvement in MDA and GSH levels and a significant decrease in IL-1β levels in rats with the excitotoxicity model. Gal-3 expressions in the hippocampus and cerebellum increased in KA-treated rats, whereas TXR treatment decreased Gal-3 expressions. In addition, histopathological changes caused by KA administration showed improvement in TXR-treated groups. In conclusion, the findings showed that TXR treatment attenuated KA-induced neurotoxicity by reducing oxidative tissue damage, inflammatory response and Gal-3 expression. Graphical Abstract