Differential susceptibility to oxidant stress (Sodium chlorite) in mice with different levels of erythrocyte G‐6‐PD activity

Abstract

Persons with glucose‐6‐phosphate dehydrogenase (G‐6‐PD) deficiency reoresent a group at increased risk to hemolytic anemia from a variety of industrial and therapeutic chemical agents. The possible role of chemicals in the ambient air and water as potential causes of hemolytic episodes in the G‐6‐PD deficient condition has not been investigated. One potential oxidant stressor is sodium chlorite which may be found in drinking water disinfected with chlorine dioxide. This is a disinfectant widely used in Europe and presently being considered for application in the U.S.A. by the Environmental Protection Agency.

When C57L/J (low G6PD activity) and A/J (high G6PD activity) mice were treated with sodium chlorite, there was very little difference between the strains in the nine hematologic parameters measured. However, when the tails of the mice were cut to obtain blood samples, a significant hemolytic crisis developed in the C57L/J strain being treated with sodium chlorite, whereas no other treatment or control group developed these responses. An explanation of the role of injury (tail cutting) in enhancing hemolysis from sodium chlorite exposure on the C57L/J strain is given. The value of the C57L/J mouse strain in simulating the human G6PD deficient condition is discussed.

Key words:

• chlorite
• oxidant
• G‐6‐PD deficiency
• copper
• ozone hemolysis
• chloramines
• chlorination
• drinking water