PMID- 3015494
OWN - NLM
STAT- MEDLINE
DCOM- 19860916
LR  - 20190828
IS  - 0271-3683 (Print)
IS  - 0271-3683 (Linking)
VI  - 5
IP  - 6
DP  - 1986 Jun
TI  - The protective effect of glucose on soluble rat lens hexokinase in the presence 
      of oxidative stress.
PG  - 433-9
AB  - An in vitro animal model was used to characterize the protective effect of 
      glucose on lenses subjected to oxidative stress. Paired rat lenses were incubated 
      in TC-199 medium for six hours in the presence of an oxidant (0.06 mM H2O2, 
      superoxide produced from 5 mM purine, or hydroxyl radical) and 2 mM glucose 
      (control) or no glucose (experimental). Soluble hexokinase (HK) specific activity 
      and lactate production were measured. 0.06 mM H2O2 inactivates 48% of the 
      hexokinase in the absence of glucose; with glucose present hexokinase activity is 
      reduced only 26%. Control experiments without oxidants show a statistically 
      insignificant difference between hexokinase activities in the 0 and 2 mM groups, 
      suggesting that the changes observed are not simply due to the presence or 
      absence of glucose. Hexosemonophosphate shunt activity increases nearly 2.5-fold 
      in the presence of 0.06 mM H2O2 and 2.0, 4.0 or 5.5 mM glucose. This suggests 
      that the loss of hexokinase (a -SH enzyme) in the presence of H2O2 and 0 mM 
      glucose is due to NADPH production inadequate to offset the oxidative stress on 
      enzyme -SH groups. FPLC analysis suggests that type II HK is more susceptible to 
      oxidative inactivation than type I, and further studies have shown that this 
      inactivation is localized to the capsule/epithelium. Lactate levels were measured 
      and controls (without oxidants) were run, to obtain a baseline value for fresh 
      lenses and assess the contribution of endogenous glucose to lactate production. 
      H2O2 levels in superoxide and hydroxyl radical media were measured, and the 
      protective effects of mannitol and catalase were also determined.
FAU - Kletzky, D L
AU  - Kletzky DL
FAU - Tung, W H
AU  - Tung WH
FAU - Chylack, L T Jr
AU  - Chylack LT Jr
LA  - eng
GR  - EY03247/EY/NEI NIH HHS/United States
GR  - EY05552/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Curr Eye Res
JT  - Current eye research
JID - 8104312
RN  - 0 (Culture Media)
RN  - 0 (Hexosephosphates)
RN  - 0 (Hydroxides)
RN  - 0 (Lactates)
RN  - 11062-77-4 (Superoxides)
RN  - 3OWL53L36A (Mannitol)
RN  - 9159UV381P (hydroxide ion)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - EC 1.11.1.6 (Catalase)
RN  - EC 2.7.1.1 (Hexokinase)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Animals
MH  - Catalase/pharmacology
MH  - Culture Media
MH  - Glucose/*pharmacology
MH  - Hexokinase/*metabolism
MH  - Hexosephosphates/metabolism
MH  - Hydrogen Peroxide/analysis/*pharmacology
MH  - Hydroxides/*pharmacology
MH  - Lactates/biosynthesis
MH  - Lens, Crystalline/*enzymology/metabolism
MH  - Male
MH  - Mannitol/pharmacology
MH  - Rats
MH  - Rats, Inbred Strains
MH  - Solubility
MH  - Superoxides/*pharmacology
EDAT- 1986/06/01 00:00
MHDA- 2001/03/28 10:01
CRDT- 1986/06/01 00:00
PHST- 1986/06/01 00:00 [pubmed]
PHST- 2001/03/28 10:01 [medline]
PHST- 1986/06/01 00:00 [entrez]
AID - 10.3109/02713688609015112 [doi]
PST - ppublish
SO  - Curr Eye Res. 1986 Jun;5(6):433-9. doi: 10.3109/02713688609015112.