Alterations in pulmonary protective enzymes following systemic bleomycin treatment in mice☆
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Cited by (49)
The role of atopy in the pathogenesis of bleomycin pulmonary toxicity
2019, Respiratory MedicineEpicatechin protective effects on bleomycin-induced pulmonary oxidative stress and fibrosis in mice
2019, Biomedicine and PharmacotherapyCitation Excerpt :The oxidative stress that activates inflammatory signaling pathways causes oxidative damage [45]. In BLM model of lung injury, oxidative damage is a condition due to the lack of balance between ROS production and the antioxidant defense system [46,47]. It has been reported that oxidative stress and inflammation are early and fibrosis is a late event in BLM model of lung damage [12,15].
Oxidative toxicology of bleomycin: Role of the extracellular redox environment
2019, Current Opinion in ToxicologyCitation Excerpt :The pyrimidine and imidazole moieties that bind oxygen and iron result in the formation of free radical species such as O2−, hydroxyl radicals and Fe (III). The bleomycin complex then binds to DNA helix through a bithiazol ring, resulting in DNA strand breaks and lipid peroxidation [9,10]. The result is an increase in cellular injury, which is then followed by an inflammatory response.
Sinapic acid ameliorates bleomycin-induced lung fibrosis in rats
2018, Biomedicine and PharmacotherapyCelastrol enhances Nrf2 mediated antioxidant enzymes and exhibits anti-fibrotic effect through regulation of collagen production against bleomycin-induced pulmonary fibrosis
2016, Chemico-Biological InteractionsCitation Excerpt :During oxidative stress, rapid over-production of free radicals overwhelms the detoxification and scavenging capacity of cellular anti-oxidant enzymes like SOD, CAT, GPx, GR and non-enzymatic antioxidants such as vitamin E, vitamin C and GSH, resulting in a severe damage to macromolecules and generate toxic lipid peroxides that ultimately leads to organ failure [11]. BLM administration in animals results in increased lipid peroxidation (LPO) and alters the activities of antioxidant enzymes in BALF and lung tissue has been documented [42]. Plant secondary metabolites act as powerful antioxidants providing a remarkable protection against oxidative and free radical damage.
Protective effect of gallic acid against bleomycin-induced pulmonary fibrosis in rats
2015, Pharmacological ReportsCitation Excerpt :Also, several studies suggested a similar relation in humans as well [10,12]. The lung is selectively influenced because this tissue lacks an enzyme that hydrolyzes the bleomycin, which prevents its metabolite from binding to metal ions and DNA [13]. The complex metabolites can generate ROS such as superoxide and hydroxyl radicals [11].
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Supported by National Institutes of Health Grants (CA-01012; CA-25883), American Cancer Society Grant CH-316, and a grant from the Parker B. Francis Foundation.
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Current address: Department of Pharmacology, 518 Scaife Hall, University of Pittsburgh, School of Medicine, Pittsburgh, PA 15261.