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From Designer Food Formulation to Oxidative Stress Mitigation: Health-Boosting Constituents of Cabbage
Published in Megh R. Goyal, Hafiz Ansar Rasul Suleria, Ramasamy Harikrishnan, The Role of Phytoconstitutents in Health Care, 2020
Faiza Ashfaq, Masood Sadiq Butt, Ahmad Bilal, Kanza Aziz Awan, Hafiz Ansar Rasul Suleria
In normal metabolic processes, Reactive Oxygen/Nitrogen Species/ Metabolites (ROSs/RNSs/ROMs) are continuously being produced, i.e., neutralized by detoxification system of antioxidants and antioxidative enzymes. In response to the over-consumption of junk food, this system is insufficient to combat free radicals. This results in the generation of ROS/ROM (superoxide anion, hydrogen peroxide, and hydroxyl ion) via numerous pathomechanisms inducing sequential events of oxidative injury especially in the fragile organs of the body [28, 139]. Basically, the over-accumulation of free radicals and their covalent bonding with bio-molecules induce peroxidative damage of lipophilic (rich in PUFA) membrane structure leading to the synthesis of lipid peroxides that are involved in multiple pathologies.
Pathology of the Liver: Functional and Structural Alterations of Hepatocyte Organelles Induced by Cell Injury
Published in Robert G. Meeks, Steadman D. Harrison, Richard J. Bull, Hepatotoxicology, 2020
Louis Marzella, Benjamin F. Trump
Phospholipid inclusions in the form of myelin figures are found in the lysosomes of patients with drug-induced lipidosis. These agents retard the degradation of lipid which normally enters the lysosomes by autophagy and heterophagy. Lysosomal degradation is inhibited by alkalinization of the lysosomal milieu by drugs (such as chloroquine) that are weak bases (Poole and Ohkuma, 1981). Some drugs such as aminoglycosides may inhibit lysosomal phospholipases (Hostetler and Hall, 1982; Regec et al., 1986). A variety of other drugs with amphiphilic structure are thought to bind to phospholipids and prevent their degradation by lysosomal enzymes (de la Iglesia et al., 1974; Dake et al., 1985). Phospholipids may become chemically altered before entry into the lysosomes. Formation of lipid peroxides may occur in large amounts during oxidative stress or slowly as cells age. These molecules are resistant to digestion and accumulate in the lysosomes as lipofuscin.
Skin Equivalents to Measure Phototoxicity
Published in Francis N. Marzulli, Howard I. Maibach, Dermatotoxicology Methods: The Laboratory Worker’s Vade Mecum, 2019
André Rougier, Catherine Cohen, Roland Roguet
Epidermal equivalents were crushed and extracted in isopropanol. Lipid peroxides were then measured using the K-Assay LPO-CC (KAMIYA Biomedical Company). Cumene hydroperoxide was used to generate standard curves to calibrate this very sensitive colorimetric test.
Investigation of the phytochemical composition and remedial effects of southern grape hyacinth (Muscari neglectum Guss. ex Ten.) plant extract against carbon tetrachloride-induced oxidative stress in rats
Published in Drug and Chemical Toxicology, 2023
Aysegul Eroglu, Abdulahad Dogan
In the in vivo section of this study, the possible effects of the compounds detected in the MAP and MB ethanol extract of M. neglectum were investigated in a rat model against CCl4 toxicity. Therefore, a rat animal model was used to induce tissue damage with CCl4 to describe the mechanisms and explore the potential treatment of the M. neglectum extracts. Exposure to CCl4 is one of the most widely used models to investigate various natural extracts (Dogan et al. 2022). CCl4 causes acute and chronic toxicity in various tissues, especially the liver, resulting in steatosis, cellular necrosis, fibrosis, and cirrhosis (Weber et al.2003). CCl4 is metabolized by cytochrome p450 to the highly reactive trichloromethyl free radical (CCl3·), which is then converted to trichloromethyl peroxy radical (CCl3OO.). Subsequently, CCl3OO. reacts with fatty acids in cell macromolecular protein and cytoplasmic membrane phospholipids to form more toxic trichloromethyl peroxyl radicals (CCl3O.). As a result, the peroxidative degradation of lipid membranes occurs, leading to the formation of lipid peroxides (Winczura et al.2012).
Protective effect of royal jelly on fluoride-induced nephrotoxicity in rats via the some protein biomarkers signalling pathways: a new approach for kidney damage
Published in Biomarkers, 2022
Abdullah Aslan, Seda Beyaz, Ozlem Gok, Muhammed Ismail Can, Gozde Parlak, Ramazan Gundogdu, Ibrahim Hanifi Ozercan, Serpil Baspinar
Oxidative stress is described as an imbalance between oxidant (free radical) production and antioxidant defense system in favour of the oxidant system. The products of the oxidant system are known as free radicals which are some reactive oxygen products such as superoxide anion, hydrogen peroxide, hydroxyl radical, peroxy radical, hydroperoxy radical. Free radicals causes damage to cellular biomolecules including nucleic acids, proteins and lipids. Radical damage to unsaturated fatty acids in cell membranes and plasma lipoproteins leads to the formation of lipid peroxides. The final product of lipid hydroperoxides, malondialdehydes (MDA), disrupt the functions of the cell by interacting with biomolecules such as nucleic acids or proteins. There is an antioxidant defense system against all these harmful effects of free radicals. Apart from enzymatic antioxidant structures such as catalase (CAT), glutathione (GSH) is an antioxidant responsible for providing non-enzymatic intracellular redox hemostasis (Kum 2017, Beyaz et al.2022a). This research revealed the therapeutical capacity of royal jelly in the treatment of various human diseases in the future by limiting kidney damage.
Effects of the methanol fraction of modified Seonghyangjeongki-san water extract on transient ischaemic brain injury in mice
Published in Pharmaceutical Biology, 2021
Eun-Jin Kang, Suin Cho, Chiyeon Lim, Byoungho Lee, Young Kyun Kim, Kyoung-Min Kim
After the initiation of ischaemia, energy depletion causes mitochondrial dysfunction and the release of ROS and reactive nitrogen species. ROS are also known to cause various diseases, such as ageing and cancer (Kehrer 1993; Ghanta et al. 2007), and their accumulation causes inflammation via the generation of harmful cell responses (Mukhopadhyay et al. 2012). MDA is a lipoperoxidation product whose levels are increased because of an increase in oxidative stress (Kotani et al. 2015). Lipid peroxide causes cell damage and ageing and alters the physiological and chemical properties of the cell membrane (Gutteridge 1995; Dawn-Linsley et al. 2005). In this study, pre-treatment with SHJKSmex effectively inhibited the increase in ROS and MDA levels caused by MCAO-induced brain injury. Furthermore, oxidative stress was significantly suppressed in the 300 mg/kg group (Figure 6). Our findings suggest that the effects of pre-treatment with SHJKSmex on ischaemic brain injury are associated with the inhibition of oxidative damage.