title: Ameliorative effect of acetyl-L-carnitine and/or nifedipine against selenite-induced cataractogenesis in young albino rats.
abstract: Free radical toxicity and calcium ion overload have been identified as the major two players in the causation of cataract. The current study was carried out to investigate the anti-cataractogenic effect of single and combined treatment with acetyl-l-carnitine and nifedipine in sodium selenite-induced cataract. Rat pups were divided into 5 groups; 1st group received intraperitoneal injection (i.p.) of saline and served as normal control, 2nd group received single subcutaneous injection of sodium selenite 30nmol/g body weight on p10 (postpartum day 10), 3rd and 4th groups received either acetyl-l-carnitine (200mg/kg, i.p.) or nifedipine (0.1mg/kg, i.p.) on p9, respectively, before the administration of sodium selenite, and the treatment continued till p14. Last group received the combined treatments of acetyl-l-carnitine and nifedipine in the same regimen. All animals were examined using a slit lamp and retroillumination then sacrificed on p30. Lenses were removed and processed for biochemical analyses, histopathological and electron microscopic examination. Selenite-treated groups showed significantly (P≤0.05) lower values of redox system components (glutathione and glutathione reductase activity) and anti-oxidant enzymes׳ activities (superoxide dismutase and catalase) along with increased lipid peroxidation that was accompanied by 100% opacified crystalline lenses (mature cataract) with abnormal structure as detected by electron microscopy. It is concluded that acetyl-l-carnitine or nifedipine was able to partially protect against selenite-induced abnormalities. While, combined treatment with acetyl-l-carnitine and nifedipine was superior to individual treatments in slowing down the development of cataract by restoring the anti-oxidant defense and mitigating lipid peroxidation in the lens and hence represents an attractive anti-cataractogenic remedy.
authors: Department of Histology, Faculty of Medicine, Suez Canal University, Ismailia 41522, Egypt.
authors: Lamiaa M
authors: LM
authors: Farghaly
authors: Department of Ophthalmology, Faculty of Medicine, Suez Canal University, Ismailia 41522, Egypt.
authors: Waleed A
authors: WA
authors: Ghobashy
authors: Department of Anatomy, Faculty of Medicine, Ain Shams University, Egypt.
authors: Youssef
authors: Y
authors: Shoukry
authors: Department of Pharmacology and Toxicology, Faculty of Pharmacy, Suez Canal University, Ismailia 41522, Egypt. Electronic address: mona_azab@hotmail.com.
authors: Mona F
authors: MF
authors: El-Azab
mesh_terms: D000108:Acetylcarnitine / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D000831:Animals, Newborn; D002386:Cataract / Q000139:chemically induced* / Q000378:metabolism / Q000517:prevention & control*; D005260:Female; D009543:Nifedipine / Q000494:pharmacology / Q000627:therapeutic use*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D020887:Selenious Acid / Q000633:toxicity*; D016896:Treatment Outcome
chemical_list: D000108:Acetylcarnitine; D020887:Selenious Acid; D009543:Nifedipine
keywords: Calcium channel blockers; Cataract; Oxidative stress; Selenite; l-Carnitine