Ethidium bromide is thought to act as a mutagen because it intercalates double-stranded DNA (i.e. inserts itself between the strands), deforming the DNA. This could affect DNA biological processes, like DNA replication and transcription. Ethidium bromide has been shown to be mutagenic to bacteria via the Ames test, but only after treatment with liver homogenate, which simulates the metabolic breakdown of the molecule being tested. The lack of detected mutagenicity without liver homogenate indicates that ethidium bromide is not directly mutagenic, but that its metabolites are; however, the identity of these mutagenic metabolites are unknown. The National Toxicology Program states it is not mutagenic in rats and mice. These conclusions are supported by a subchronic carcinogenicity study in mice, whereby no mutagenic effects were detected. Ethidium bromide (Homidium brand) use in animals to treat trypanosome infection suggests that toxicity and mutagenicity are not high. Studies have been conducted in animals to evaluate EtBr as a potential antitumorigenic chemotherapeutic agent. Its chemotherapeutic use is due to its toxicity to mitochondria. A more recent study shows that EtBr acts as a topoisomerase I poison, just like several anticancer drugs used in humans. The above studies do not support the commonly-held idea that ethidium bromide is a potent mutagen in humans, but they do indicate that it can be toxic at high concentrations. Recent science writers have reported on what is perceived to be disproportionate fear over the toxicity and mutagenicity of the compound.