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Protective effect of Naringenin against Arsenic trioxide induced oxidative stress
Author(s) -
Peruru Rupa Sree,
Dodoala Sujatha
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb577
Subject(s) - naringenin , oxidative stress , arsenic trioxide , chemistry , arsenic , neuroprotection , neurodegeneration , pharmacology , arsenic toxicity , antioxidant , biochemistry , medicine , flavonoid , disease , organic chemistry
Arsenic is a heavy metal and a well known environmental pollutant especially as a ground water pollutant in various parts of the world. The increasing risk of chronic exposure to arsenic globally has been alarming and many health complications were reported upon long‐term subjection to arsenic including cardiovascular disorders, metabolic disorders, diabetes mellitus, neurodegenerative disorders, developmental abnormalities and so forth. Arsenic in its inorganic form (iAs) is more harmful than organic form. Inorganic arsenic exists in trivalent and pentavalent forms, the trivalent meta arsenite (As +3 ) is the most toxic form. Arsenic induced neurodegeneration is still a thrust area where a quality research is required for the development of good treatment options. The modes of action of arsenicals are quite complicated but induction of oxidative stress is the major underlying mechanism for its neuronal damage. Here, the current study has demonstrated that iAs significantly increased the oxidative stress levels in various parts of the brain lead to neuronal damage. Naringenin is a flavonoid widely reported for its strong antioxidant and neuroprotective properties. So naringenin was selected as a pharmacological intervention to target arsenic induced neurodegeneration. The brain tissues were incubated with both 10mM As 2 O 3 and 10 – 100 μm of naringenin. In the current work, the rat brain was incubated in vitro with arsenic trioxide (As 2 O 3 ) and naringenin in various patterns. The whole brain, brain slices and specific parts of the brain like frontal cortex, corpus striatum and hypothalamus were incubated separately with 10 mM As 2 O 3 (As +3 ) for 30 min in artificial cerebrospinal fluid. Then oxidative stress and protein degeneration parameters were estimated from the homogenates. The tissue damage levels were evaluated by measuring the extent of lipid peroxidation and the formation of protein carbonyls. These levels were increased significantly as compared to that of the normal. It was observed that, a fall in the levels of antioxidant enzymes like superoxide dismutase, reduced glutathione and catalase on arsenic treatment. The total protein content of the tissue homogenate was less compared to normal. Treatment with the naringenin effectively reversed these iAs‐induced responses. The lipid peroxidation and formation of protein carbonyl was found to be decrease and the protective antioxidant enzyme levels were increased when compared to arsenic alone treatment. The total protein content also significantly increased. By this it is concluded that naringenin is effectively working against arsenic induced neuronal damage. Naringenin can be developed as a potent therapeutic option in the treatment of arsenic induced neuronal damage. Further studies will be carried out using suitable in vivo animal model to understand the effect of naringenin in Arsenic trioxide induced neurotoxicity. Support or Funding Information Sri Padmavati Mahila Visvavidyalayam, Tirupati, Andhra Pradesh, India. Department of Science and Technology (DST), Government of India.