Acute patho-toxicological indicators of methaemoglobinemia

Abstract

Methaemoglobin is formed when the haem iron of deoxyhaemoglobin is oxidized from its ferrous (Fe2+) to the ferric state (Fe3+) resulting in a haemoglobin molecule that is structurally and functionally altered, which leads to tissue hypoxia and metabolic acidosis. Classifications of methaemoglobinemia are based on clinical history, causative agents, pattern of transmission and optical spectrum presentation of blood specimen and level of erythrocyte NADH-methaemoglobin reductase activity. Two major types of molecular/metabolic events leading to the presentation of methaemoglobinemia have been identified. The majority of the chemically induced-methaemoglobinemias are outcome of the presence of relatively high concentrations of oxidizing agents that overwhelm protective cellular reductive capacity of NADH-methaemoglobin reductase activity rather than inhibition of the enzyme. The control of physiologic levels of methaemoglobin is intricately intertwined with glucose metabolism for the supply of NADH and NADPH to provide electrons and protons for enzymatic reduction of methaemoglobin in concert with auxiliary antioxidant systems. The management and amelioration of methaemoglobinemia involves exchange transfusion and/or methylene blue administration.

Keywords

• Methaemoglobin
• Methaemoglobinopathies
• NADH-methaemoglobin reductase
• Nitrate
• Nitrite