title: Merit of quinacrine in the decrease of ingested sulfite-induced toxic action in rat brain.
abstract: We aimed at investigating the effects of sulfite-induced lipid peroxidation and apoptosis mediated by secretory phospholipase A2 (sPLA2) on somatosensory evoked potentials (SEP) alterations in rats. Thirty male albino Wistar rats were randomized into three experimental groups as follows; control (C), sodium metabisulfite treated (S), sodium metabisulfite+quinacrine treated (SQ). Sodium metabisulfite (100 mg/kg/day) was given by gastric gavage for 5 weeks and 10 mg/kg/day quinacrine was applied as a single dose of intraperitoneal injection for the same period. The latencies of SEP components were significantly prolonged in the S group and returned to control levels following quinacrine administration. Plasma-S-sulfonate level was increased in S and SQ groups. TBARS levels in the S group were significantly higher than those detected in controls. Quinacrine significantly decreased brain TBARS levels in the SQ group compared with the S group. Quinacrine treatment did not have an effect on the increased sPLA2 level of the sulfite administered group. Immunohistochemistry showed that sulfite caused an increase in caspase-3 and TUNEL positive cells, restored to control levels via quinacrine administration. This study showed that sPLA2 might play a role in ingested sulfite-induced SEP alterations, oxidative stress, apoptotic cell death and DNA damage in the brain.
authors.affiliation: Akdeniz University, Medical School, Department of Biophysics, Antalya, Turkey.
authors.forename: Ceren
authors.initials: C
authors.lastname: Kencebay
authors.forename: Narin
authors.initials: N
authors.lastname: Derin
authors.forename: Ozlem
authors.initials: O
authors.lastname: Ozsoy
authors.forename: Dijle
authors.initials: D
authors.lastname: Kipmen-Korgun
authors.forename: Gamze
authors.initials: G
authors.lastname: Tanriover
authors.forename: Nihal
authors.initials: N
authors.lastname: Ozturk
authors.forename: Goksun
authors.initials: G
authors.lastname: Basaranlar
authors.forename: Piraye
authors.initials: P
authors.lastname: Yargicoglu-Akkiraz
authors.forename: Berna
authors.initials: B
authors.lastname: Sozen
authors.forename: Aysel
authors.initials: A
authors.lastname: Agar
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D001921:Brain / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D053148:Caspase 3 / Q000378:metabolism; D005071:Evoked Potentials / Q000187:drug effects; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D054497:Phospholipases A2, Secretory / Q000378:metabolism*; D011796:Quinacrine / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013447:Sulfites / Q000008:administration & dosage / Q000633:toxicity*; D013451:Sulfonic Acids / Q000097:blood; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D013447:Sulfites; D013451:Sulfonic Acids; D017392:Thiobarbituric Acid Reactive Substances; C005200:sodium metabisulfite; D054497:Phospholipases A2, Secretory; D053148:Caspase 3; D011796:Quinacrine