Carbon monoxide‐induced brain injury: Neurochemical studies after single and repeated exposures

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Abstract
Biochemical effects of a single and once‐repeated exposure to carbon monoxide (0.2% CO, 30 min) were studied in mouse brain. The effect of the severity of the first exposure on the brain reaction to the second exposure (0.2% CO, 30 min) was also studied after exposure to four different CO doses (0.2% CO for 0, 2 or 5 h, and 0.3% CO for 2 h). 1. The DNA content of brain decreased after single and once‐repeated CO exposures. The effect of the second exposure was greater than that of the first. 2. The changes in the glycosphingolipid synthesis of brain were measured as the specific rate of precursor incorporation into the two isolated galactolipid fractions, i.e., cerebrosides and gangliosides following a 2‐h pulse‐labelling with 3H‐galactose in vivo. The synthesis of cerebrosides was substantially inhibited for a short period after the first and the second exposures. A late compensatory over‐ecovery of synthesis was found only after the second exposure. The rate of galactose incorporation into gangliosides was not immediately depressed after CO exposure, but otherwise the changes were similar to those of cerebrosides. 3. The protein, phospholipid and cerebroside contents of brain were also affected in parallel fashion with the changes of DNA content. The content of gangliosides was increased after the first, but not after the second exposure. The enhanced reaction of brain to the second CO poisoning suggests the existence of sublethal brain cell injury which is produced by the first CO exposure and manifested by altered reactions to the second exposure.