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Airway Repair and Adaptation to Inhalation Injury
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
S. F. Paul Man, William C. Hulbert
The role of dietary interventions such as vitamin E and selenium against tissue injury by oxidizing gases has been addressed by several investigators (Goldstein et al., 1970; Menzel et al., 1972; Elsayed et al., 1983; McMillan and Boyd, 1982). It has been postulated that the antioxidant properties may be the result of vitamin E being preferentially oxidized by the oxidizing gas, thereby preventing the formation of lipid peroxides, or vitamin E may react with free radicals produced by lipid peroxidation (Tappel, 1982).
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.
Natural Products as Economical Agents for Antioxidant Activity
Published in Hafiz Ansar Rasul Suleria, Megh R. Goyal, Masood Sadiq Butt, Phytochemicals from Medicinal Plants, 2019
Nida Nazar, Abdullah Ijaz Hussain, Syed Makhdoom Hussain, Poonam Singh Nigam
Glutathione, another important antioxidant, can directly suppress the oxidative effects of ROS like lipid peroxides, and thus plays main role in xenobiotic metabolism. The study has shown that vitamin C and glutathione jointly act as antioxidant and thus reduce the free radicals and have a sparing effect upon each other.77 Natural antioxidants, in pure or concentrated form, such as CQ-10, L-arginine, and melatonin, have recently been used as supplements for the treatment and prevention of various diseases especially, chronic and degenerative diseases.118
Role of Oxidative Stress and the Protective Effect of Fermented Papaya Preparation in Sickle Cell Disease
Published in Hemoglobin, 2022
Prashant P. Warang, Nikhil S. Shinde, Vinod D. Umare, Prajyot V. Deshmukh, Kanjaksha Ghosh, Manisha R. Madkaikar, Roshan B. Colah, Malay B. Mukherjee
Increased ROS levels destroy and alter lipid structure, leading to the formation of lipid peroxides. Therefore, determination of LP levels gives an idea of the extent of oxidative damage in the cells. In our study, lipophilic fluoresceinated phosphoethanolamine (fluor-DHPE) was used to monitor LP. As the peroxidation initiates, the fluorescence of the dye gets diminished upon reaction with peroxyl radicals. Untreated RBCs of sickle cell disease patients showed significantly more LP than normal individuals. On AAPH exposure, the fluorescence fluor-DHPE from both normal and sickled RBCs was reduced. When FPP-treated, both red cell types were exposed to AAPH, a significant rise in fluor-DHPE fluorescence was seen compared to that of untreated red cells exposed to AAPH. Earlier studies have shown that the oral administration of FFP for 4 weeks decreased the elevated lipid peroxide and increased superoxide dismutase activity in iron-induced epileptogenesis in rats [8]. Fermented papaya preparation (6 gm/d) supplementation for 12 weeks in patients with Hb E/β-thal prevented LP as well as reduced other oxidative stress markers [9].
Vitamin E for the management of major depressive disorder: possible role of the anti-inflammatory and antioxidant systems
Published in Nutritional Neuroscience, 2022
Luana M. Manosso, Anderson Camargo, Alcir L. Dafre, Ana Lúcia S. Rodrigues
Many studies have suggested that MDD is associated with oxidative and nitrosative stress [70,71,78–80]. Of note, a study reported that increased malondialdehyde content (a lipid peroxidation marker) and antioxidant enzyme activities in the blood of patients with MDD returned to normal values after treatment for three months with selective serotonin reuptake inhibitors [81]. Another study showed a positive correlation between the oxidative stress index and the severity of MDD evaluated by the Hamilton Depression Rating Scale (HDRS) values [82]. Additionally, a positive correlation between lipid peroxides and depressive symptoms (assessed by the Center for Epidemiologic Studies Depression scale – CES-D) was previously demonstrated, suggesting that lipid peroxidation is related to MDD [83]. Furthermore, a compelling study demonstrated that patients with MDD present increased plasma levels of malondialdehyde and superoxide dismutase activity, an effect more prominent in severe MDD [84]. Conversely, reduced superoxide dismutase activity in the serum of patients with MDD was also reported, an effect paralleled by increased oxidative stress markers [78].
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.