Japanese
 NBRP Rat No: 0081 Strain Name: SHR.ODS-Gulood/Shi Commmon Name: SHR.ODS-<i>Gulo<sup>od</sup></i>, SHR-od
 Principal Investigator  Tsutomu Hirasawa
 Organization   Shionogi & Co., Ltd.  Aburahi Laboratories
 Address  1405, Gotanda, Koka-cho, Koka-gun

520-3423 Shiga

 JAPAN
 Telephone  0748-88-3281  Fax:  0748-88-2783  srp-contact@shionogi.co.jp
 Inbred Generations   F36 (May 2009) 
   
 Coat Color
 Deposition Status
 
 albino (c)
  Embryo      Sperm      Live Animals
 Usage Restrictions  The recipient of BIOLOGICAL RESOURCE shall obtain a prior written consent on use of it from the DEPOSITOR.
Use of the BIOLOGICAL RESOURCE shall be limited to a collaborative research with the DEPOSITOR. 
 Genetic Status   Inbred   Segregating   Congenic   Consomic    Recombinant 
  Coisogenic   Spont. Mutant    Transgene   Ind. Mutant    Others 
 Comercial Availability   
 Research Category   Diabetes Obesity    Neurobiology    Ophthalmology    Dentistry    Cardio- Hypertension 
  Oncology   Metabolism   Otorhinology    Immunology    Infectious Disease
  Osteology    Internal Medicine   Dermatology   Reproduction    Development
  Behavior    Hematology    Urology   Pharmacology   Others 
  Control Strains   Reporter gene Strains  
 Gene Gulo: gulonolactone (L-) oxidase
 Origin A congenic strain developed from a recipient, SHR(Spontaneously Hypertensive Rat) and a donor, ODS (Lack of L-gulono-gamma-lactone oxidasestrainin). Introduced to Nagoya University in 1995 (now F18).
 
 Strain Characteristics The osteogenic disorder Shionogi (ODS) rat is a mutant Wistar rat that is subject to scurvy, because it lacks L-gulono-gamma-lactone oxidase, a key enzyme in L-ascorbic acid biosynthesis (Horio et al. 1985) 
 Breeding Conditions Normal breeding when L-ascorbic acid is supplemented in food (1000mg/kg) or water (1g/L). Breeding performance is unclear post 3rd delivery. 
 Genotyping PCR-RFLP 
 References  Horio F, Hayashi K, Mishima T, Takemori K, Oshima I, Makino S, Kakinuma A, Ito H.
A newly established strain of spontaneously hypertensive rat with a defect of ascorbic acid biosynthesis.
Life Sci. 2001 Sep 7;69(16):1879-90.

Kawai K, Ito H, Kubota H, Takemori K, Makino S, Horio F.
Changes in catecholamine metabolism by ascorbic acid deficiency in spontaneously hypertensive rats unable to synthesize ascorbic acid.
Life Sci. 2003 Feb 28;72(15):1717-32.