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    It has been suggested that these metabolic pathways are readily saturated in children as well as adults leading to the accumulation of an otherwise minor nontoxic metabolite that may become responsible for hepatic injury (31). Ultrastructural changes include increased numbers of lysosomes, peroxisomes, and mitochondria with dilation of the smooth and the rough endoplasmic reticulum (25). Aspirin injury is both dose- and blood concentration–dependent consistent with intrinsic toxicity as seen in both animals and cell culture experiments.

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