Abstract:The aim of this study was to investigate the difference in the serum malondialdehyde (MDA), glutathione (GSH), and nitric oxide (NO) levels between normal and T. gondii-infected patients. To this end, MDA, GSH, and NO levels in the sera of 37 seropositive patients and 40 participants in the control group were evaluated. In Toxoplasma ELISA, IgG results of the patient group were 1,013.0 ± ± 543.8 in optical density (mean ± ± SD). A statistically significant difference was found between patients and the control group in terms of MDA, GSH, and NO levels. A decrease in GSH activity was detected, while MDA and NO levels increased significantly. Consequently, it is suggested that the use of antioxidant vitamins in addition to a parasite treatment shall prove useful. The high infection vs control ratio of MDA and NO levels probably suggests the occurrence as a mechanism of tissue damage in cases of chronic toxoplasmosis. Moreover, it is recommended that the patient levels of MDA, GSH, and NO should be evaluated in toxoplasmosis.
Methyl parathion (MP) is an organophosphate chemical agent. Due to low solubility and bioaccumulation, it results in serious health problems. Electrochemical recognition based on graphitic carbon nitride (CN) incorporated hexagonal boron nitride (HBN) nanosheets and molecularly imprinted polymer (MIP) was presented for methyl parathion (MP) detection. Scanning electron microscopy (SEM), X-ray diffraction (XRD) method, cyclic voltammetry (CV) and electrochemical impedance spectroscopy (EIS) were utilized for characterizations. After that, MP imprinted voltammetric sensor on CN-HBN nanocomposite was carried out in the presence of 100.0 mM pyrrole containing 25.0 mM MP via CV. 1.0 × 10 −12 -2.0 × 10 −9 M and 2.0 × 10 −13 M were found as the linearity range and the detection limit (LOD). Finally, MP imprinted sensor was applied to orange juice samples for MP analysis.
The increase in the formation of reactive oxygen and reactive nitrogen species of endogenous or exogenous origin causes oxidative stress due to pro-oxidant and antioxidant imbalance that causes cellular damage in metabolism. This can increase inflammation of cells, apoptosis and necrosis, damage to DNA base damage, DNA and protein cross-links, lipid membrane peroxidation, and mitochondrial dysfunction. Antioxidants can be described as a system that protects biomolecules and the organism against the harmful effects of free radicals, reduces or repairs the damage done by reactive oxygen species (ROS) to the target molecule, and this is called antioxidant defense. It is known that the mechanisms caused by the increase in ROS resulting from oxidative stress are positively related to the pathology of many diseases such as cancer, metabolic syndrome, atherosclerosis, malaria, Alzheimer’s disease, rheumatoid arthritis, neurodegenerative diseases and preeclampsia.
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