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Ganoderma lucidum is also known as Lingzhi or Reishi, have long been used in China, Japan, and other Asian nations to promote longevity and good health. Reishi is uncommon among farmed mushrooms in that its medicinal rather than nutritional value is critical. Commercial Reishi products come in a number of forms, including powders, nutritional supplements, and tea. These preparations are produced from different parts of the fungus, including the fruit body, spores, and mycelıa. Specific applications and health advantages of Reıshı include blood sugar regulation, hepatoprotection, immune system modulation, bacteriostasis, and more. A variety of Reishi products made from various portions of the fungus are currently available on the market. The most basic version is comprised of entire cork bodies reduced to powder and then processed into capsules or tablets. In this study, the comparison and examination of antioxidant activity in Reishi tablets and powdered teas of different brands sold in Türkiye was carried out using DPPH, DMPD, and Folin Ciocalteu methods. According to the results we obtained in our study, from aqueous mushroom extracts; It was observed that N5, N1, and N2 (259.8696 µgGAE/mL, 220.1594 µgGAE/mL, 185.6667 µgGAE/mL) samples had high phenolic content, while N3 and N4 (80.01449µgGAE/mL, 119.2899 µgGAE/mL) samples had low phenolic content. Antioxidant scavenging capacities were found in parallel with the phenolic contents of the samples and the percentage scavenging capacities of DMPD/EtOH, DMPD/water, and DPPH/EtOH. IC50 values for DMPD aqueous extracts are 0.155 mg/ml (N1), 1.704 mg/ml (N2), 7.453 mg/ml (N3), 6.570 mg/ml (N4), 2.223 mg/ml (N5); For ethanolic extracts, it is 0.138 mg/ml (N1), 1.496 mg/ml (N2), 2.796 mg/ml (N3), 4.780 mg/ml (N4), 2.162 mg/ml (N5). IC50 values could not be calculated due to high DPPH results. [ABSTRACT FROM AUTHOR]

Since patients with triple-negative breast cancer do not respond to hormone therapy, the main treatment method is the combination of chemotherapy and radiotherapy. Because the DNA of the tumor cell is the target in both some chemotherapeutics and radiotherapy, problems may occur in individuals with a high DNA repair pathway. It is suggested that high expression of the Tip60 gene, which has an important role in repairing DNA damage, will increase the repair of DNA double-strand breaks in tumor cells, especially during radiotherapy treatment, thus reducing the response to treatment and adversely affecting treatment. In this study, for the first time, the role of the silenced and active Tip60 gene in response to radiotherapy in MDA-MB-231 and MCF-7 cells was investigated. For this purpose, the Tip60 gene was silenced by applying siRNA to the cell lines and UV was applied. In the study, cytotoxicity and DNA breaks were measured by MTT and COMET methods, and mRNA and protein expression values were measured by PCR and Raman spectrophotometer in silenced, unsilenced, UV-treated, and non-UV-treated cell lines. According to the results of the study, increased DNA damage was observed in MCF-7 cell lines in which the Tip60 gene was silenced, and radiotherapy was applied, compared to the cell lines with the Tip60 gene active. It was observed that DNA damage in MDA-MB-231 cell lines was less than in cell lines with the active Tip60 gene. • TNBC is with a heterogeneous tumor structure, exhibits different biological behaviors, and has multiple molecular subtypes. • One of the most important problems encountered in chemotherapy and radiotherapy treatment is that the tumor tissue does not respond to treatment at all or less. • The combination of chemotherapy and radiotherapy may be a problem in individuals with highly active DNA repair pathways. • The over-expression of Tip60 may affect the treatment by repairing DNA damage in tumor cells, especially in response to radiotherapy, during the treatment stages of cancer. [ABSTRACT FROM AUTHOR]

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Oxidative stress plays an important role in the degeneration of dopaminergic neurons, which causes Parkinson's disease (PD). Oxidative stress products, antioxidant and their balance have important roles in the development of oxidative stress‐based PD. The impact of reactive oxygen species (ROS) and defence systems can be altered by genetic polymorphisms, and thus the risk of PD may also be affected. We aimed to investigate the possible association of individual susceptibility with the development of oxidative stress‐based PD. For this purpose, we measured serum levels of folic acid, homocysteine, Vitamin B6 and B12 that play roles in folate‐dependent one‐carbon pathway, oxidant or antioxidant enzymes (NADPH oxidase, MnSOD, GPX), 8‐OHdG and repair enzymes (OGG1, XRCC1 and MTH1) by ELISA, and analysed related gene polymorphisms by PCR‐RFLP. XRCC1, ROS, NADPH and folic acid levels were found to be statistically higher in patients than controls. XRCC1, MnSOD and GPX activities were increased. We observed higher levels of 8‐OHdG in patients with MnSOD and XRCC1 mutant genotypes and higher XRCC1 levels in patients with NOX p22 fox mutant genotypes rather than controls. We suggest that routinely clinical validation of major oxidative stress‐related biomarkers will be a good approach to manage detrimental effects of PD. [ABSTRACT FROM AUTHOR]

Objective: The gamma-glutamyl cycle catalyzed by gamma-glutamyl transferase (GGT) plays an important role in glutathione (GSH) homeostasis in the cell. In cells continuously exposed to the drug, the main phase of the enzymatic detoxification is the conjugation of the drug with GSH catalyzed by glutathione-S-transferase (GST). Conjugation of drugs with GSH is the first step in the development of chemotherapeutic drug resistance. In this study, we aimed to investigate the relationship between GGT and GSH in molecular subgroups of breast cancer patients. Materials and Methods: Serum GGT activity and GSH levels for patients diagnosed with breast cancer (n=58) and healthy controls (n=8) were measured by a spectrophotometric method and a colorimetric kit, respectively. Results: GGT activity was significantly higher in the total patient group and in the molecular subgroups than those in the control groups (p<0.05). Serum GSH levels were higher in the patient groups compared to controls without reaching statistical significance (p>0.05). GGT activity was positively correlated with GSH levels in the total patients and healthy controls (p<0.001 and p<0.05, respectively). There was also a positive correlation between GGT activity and GSH levels in Luminal A, HER2-positive (Human epidermal growth factor receptor 2), and Triple-negative groups (p<0.05). Conclusion: This is the first study showing the relationship between GGT and GSH in molecular subgroups of breast cancer. An increase in GGT activity may affect intracellular GSH synthesis. Therefore, having a correlation between GGT and GSH in some molecular subgroups may affect the course of treatment in these patients. [ABSTRACT FROM AUTHOR]