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The formation of either RSeHgCH₃ or RSeHgSeR, besides neutralizing the toxicity of E + Hg forms, can accelerate the decomposition of selenium compounds to the inorganic HgSe.[ 358 , 359 , 360 ] Regarding the behavior of diphenyl diselenide in rodents exposed to CH₃Hg + or Hg 2+ , the species and the temporal relationship between the exposure to diselenide and the E + Hg influenced considerably the toxicity of Se‐ and Hg‐containing compounds.[ 349 , 350 , 351 , 361 , 362 , 363 , 364 , 365 ] For instance, quite different metabolic pathways between mice and rats were observed

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All this because rapamycin and its rapalogs selectively target only mTORC1 without affecting mTORC2, such selective inhibition could prompt feedback loops resulting in AKT activation at ser473 (216)