VanBerkum M F, Wong Y L, Lewis P N, Crapper McLachlan D R
Neurochem Res. 1986 Sep;11(9):1347-59. doi: 10.1007/BF00966128.
The yields of total and poly(A) RNA were examined in rabbit forebrains during an experimentally induced aluminum encephalopathy. Rabbits (35 day old) were injected intracranially with 13 mumole Al lactate and sacrificed 1, 3, 7, 10, or 12 days later. IRNA yields (total RNA minus transfer RNA) were not significantly altered during the encephalopathy. Poly(A) RNA yields, assayed by oligo(dT)-cellulose fractionation and by a [3H]poly(U) hybridization assay on IRNA, were increased significantly by the end of the asymptomatic stage of the encephalopathy (7 days post-Al injection). The increase in messenger RNA population may represent either a compensatory response to cell damage induced by aluminum or the accumulation of messenger RNA for proteins directly related to the expression of aluminum toxicity.
