Prof. Elie Beit-Yannai

Prof. Elie Beit-Yannai Profile

Associate Professor
Ph.D. 1999

Department : Clinical Biochemistry and Pharmacology
School of Pharmacy
Room : 522
בנין מעבדות מחקר רפואה ע"ש דייכמן - פלאם
Phone : 972-8-6477352
Email :
Office Hours :  
glaucoma, amd, antioxidants, free radicals, oxidative stress


  • 1999 Ph.D. School of Pharmacy , The Hebrew University Jerusalem

Research Interests

  • Free Radicals mediated damage, Glaucoma, Aged Macular Degeneration The role of oxidative stress in the pathophysiology of optic nerve degeneration diseases.
  • Cyclic Voltammetry as a tool for evaluation of reducing capacity in biological systems
  • Patents
    International Patent Application No. WO 02/11666 ; published on 14 February 2002. Title: DERIVATIVES OF BRANCHED-CHAIN LIPOPHILIC MOLECULES AND USES THEREOF Inventors: KOZAK Alexander, VINNIKOVA Marina, POLYAK, Michael, BEIT-YANNAI, Eliezer, REZNITSKY-COHEN, Dalia, SENDERIKHIN, Alexander

Research Projects

  • Signaling molecule within the aqueous humor in glaucoma and catarct. Looking for the role of the MAPK proteins and phosphatses in the aqeous humor.
  • Antioxidants content in new citrus hybrides cultivated in the Negev.

Research Abstract

  • My interest in oxidative stress finds expression in two research arms of my lab: 1) reactive oxygen species (ROS)-mediated glaucoma pathology, and 2) antioxidant contents in new agricultural crops. In keeping with your professional orientation I will focus here on the former. The need for new approaches in the treatment of glaucoma is the driving force behind my research. In the past few years, my lab has explored the idea that the aqueous humor (AH) serves as a medium for signaling messages and, as such, can reflect changes occurring in the surrounding tissues, as indicated by the following studies.
  • Using a congenital glaucomatic rabbit model and applying a cyclic voltammetry approach, we were able to demonstrate significant changes in the reducing capacities of the AH. These changes were attributed mainly to a drop in the concentrations of uric acid and ascorbic acid in the AH.
  • One of the consequences of oxidative stress is MAPK activation. In a rat model of induced elevated intraocular pressure (obtained by weekly intra-anterior chamber injections of hyaluronic acid), we were the first to show that Erk and JNK can be found in their active phosphorylated and general forms in the AH. In addition, in this rat model, there were marked changes in these signaling proteins, accompanied by a significant decrease in iNOS.
  • Phosphatases are known to balance kinase activity in many biological systems. I posited that the presence of kinases in the AH might be accompanied by that of different phosphatases. I found that the activities of two serine/threonine phosphatases and of protein tyrosine phosphatases were significantly higher in the AH of glaucomatic rabbits than in control rabbits.
  • An analysis of AH samples obtained from patients with cataracts vs. patients with cataracts + glaucoma showed active phosphatases in the AH in the majority of the latter samples (manuscript in preparation). The current efforts of my laboratory are now being directed towards exploring the source of these active proteins (MAPK & phosphatases). Our working hypothesis is that in response to oxidative stress and/or to elevated intraocular pressure invading macrophages might be the source. We suggest that these signaling proteins could constitute a new target for intervention, thereby opening new possibilities for the management of intraocular pressure.

Research Topics

  • Tissue communication within the ocular drainage system
  • Reactive oxygen species role in ophthalmology neurodegenerative diseases
  • Oxidative stress and antioxidants capacity in biological and agricultural system

Major expertise and techniques in the lab

  • In-vivo & in-vitro glaucoma models
  • Antioxidant capacity analysis by spectroscopic, florescent, electrochemical end enzymes approaches

Publications and funding summary / representative publications and grants

  • Beit-Yannai, E.; Trembovler, V.; Solomon, A. S., Decrease in reducing power of aqueous humor originating from glaucomatous rabbits. Eye 2007, 21, (5), 658-64. (CI 3; IF 1.974, JR 20/55 Ophthalmology)
  • Beit-Yannai, E.; Shmulevich, A., Differential Modulation of MAPKs in Relation to Increased Intraocular Pressure in the Aqueous Humor of Rat Eye Injected with Hyaluronic Acid. Current Eye Research 2009 , 34,(6), 466 – 475. (IF 1.513; JR 28/55 Ophthalmology)
  • Fleisher-Berkovich, S.; Abramovitch-Dahan,.; Ben-Shabat, S.; Apte, R.; Beit-Yannai, E. Inhibitory effect of carnosine and N-acetyl carnosine on LPS-induced microglial oxidative stress and inflammation Peptides 2009 , 30(7), 1306-1312. (CI 2; IF 2.654; JR 99/254 Pharmacology & Pharmacy)
  • Latarya, G.; Manosur, A.; Epstein, Cotlear, D.; Pikkel, J.; Levartovsky, S.; Yulish, M.; Beit-Yannai, E., Human Aqueous Humor Phosphatase Activity in Cataract and Glaucoma. Investigative ophthalmology & visual science , 2012 Feb 8. [Epub ahead of print] (IF 3.933; JR 5/55 Ophthalmology
  • Funding 20010-2012 Israel Ministry of Health: "Evaluation of the phosphatases role in the aqueous humor of glaucoma patients."

Existing collaborations

  • Dr S. Levartvsky – Human aqueous humor as a signaling medium
  • Professor AS Solomon – Congenital glaucomatic rabbit as a model for elevated IOP glaucoma
  • Dr E. Raveh - Selecting new citrus hybrids according to fruit quality
  • Dr H. Yasour - Heat damage in pepper: effects on fruit quality & nutritional values.