title: Vitamin C supplementation reconstitutes polyfunctional T cells in streptozotocin-induced diabetic rats.
abstract: BACKGROUND
  Studies have demonstrated that vitamin C supplementation enhances the immune system, prevents DNA damage, and decreases the risk of a wide range of diseases. Other study reported that leukocyte vitamin C level was low in diabetic individuals compared with nondiabetic controls.
  
  
  OBJECTIVE
  To study the effect of vitamin C on oxidative stress, blood lipid profile, and T-cell responsiveness during streptozotocin (STZ)-induced type I diabetes mellitus.
  
  
  METHODS
  Thirty male Sprague-Dawley rats were randomly split into three groups. The first served as a control group (n = 10) in which rats were injected with the vehicle alone. The second (n = 10) and the third groups (n = 10) were rendered diabetic by intraperitoneal (i.p.) injection of single doses of STZ (60 mg/kg body weight). The third group was supplemented with vitamin C (100 mg/kg body weight) for 2 months.
  
  
  RESULTS
  T lymphocytes from the diabetic rats were found to be in a stunned state, with a decreased surface expression of the CD28 costimulatory molecule, low levels of phosphorylated AKT, altered actin polymerization, diminished proliferation and cytokine production, and, eventually, a marked decrease in abundance in the periphery. Vitamin C was found to significantly decrease the elevated levels of blood hydroperoxide, glucose, cholesterol, triglycerides and low-density lipoprotein (LDL) in diabetic rats. Furthermore, it was found to restore CD28 expression, AKT phosphorylation, actin polymerization, and polyfunctional T cells (IFN-γ- and IL-2-producing cells that exhibit a high proliferation capacity).
  
  
  CONCLUSIONS
  Vitamin C treatment restores and reconstitutes polyfunctional, long-lived T cells in diabetic rats.
authors.affiliation: Zoology Department, College of Science, King Saud University, P.O. Box 2455, Riyadh, 11451, Saudi Arabia. badr73@yahoo.com
authors.forename: Gamal
authors.initials: G
authors.lastname: Badr
authors.forename: Samir
authors.initials: S
authors.lastname: Bashandy
authors.forename: Hossam
authors.initials: H
authors.lastname: Ebaid
authors.forename: Mohamed
authors.initials: M
authors.lastname: Mohany
authors.forename: Douaa
authors.initials: D
authors.lastname: Sayed
mesh_terms: D000818:Animals; D000975:Antioxidants; D001205:Ascorbic Acid / Q000008:administration & dosage*; D015153:Blotting, Western; D018106:CD28 Antigens / Q000235:genetics / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects; D004249:DNA Damage / Q000187:drug effects; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000503:physiopathology; D019587:Dietary Supplements; D015536:Down-Regulation; D007107:Immune System / Q000187:drug effects; D007371:Interferon-gamma / Q000378:metabolism; D007376:Interleukin-2 / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D010766:Phosphorylation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012307:Risk Factors; D015398:Signal Transduction; D013311:Streptozocin / Q000009:adverse effects; D013601:T-Lymphocytes / Q000187:drug effects* / Q000378:metabolism; D014280:Triglycerides / Q000097:blood; D014815:Vitamins / Q000008:administration & dosage*
chemical_list: D000975:Antioxidants; D018106:CD28 Antigens; D007376:Interleukin-2; D008077:Lipoproteins, LDL; D014280:Triglycerides; D014815:Vitamins; D013311:Streptozocin; D007371:Interferon-gamma; D001205:Ascorbic Acid