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Alternatively, one might imagine that, if an ancestral metazoan evolved a TGR enzyme that could replace both the ancestral TrxR and Gsr activities, as the version does, then perhaps the ancestral type TrxR and the ancestral Gsr were simply and irrevocably lost as being redundant with the new bi-functional TGR enzyme, as seen in

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Oxidative stress, mitochondrial dysfunction and glutamate excitotoxicity may also interact as a feed-forward vicious cycle (Nguyen et al, 2011) : Our results conclusively demonstrate that not only glutamate excitotoxicity and/or oxidative stress alters mitochondrial fission/fusion, but that an imbalance in mitochondrial fission/fusion in turn leads to NMDA receptor upregulation and oxidative stress

Glial-neuron crosstalk in health and disease: A focus on metabolism, obesity, and cognitive impairment