Gene results in terms of number seem to follow the steepness of the reproduction doseresponses curves as observed for the different chemicals but it is difficult to fully overview under the present test design. As shown in the Venn diagram, certain gene responses were shared by all three pesticide exposures or by two of them. Due to the fact that E. albidus does not have a sequenced genome, many of the significant transcripts have no similarity to known proteins. Hopefully, with future sequencing Oxybutynin chloride efforts and with the growing genomic data on invertebrate species, more transcripts will be annotated. Dimethoate affected transcripts related with sarcomere organization, maintenance of cell polarity and response to calcium ion. These transcripts code for several actin, calponin, toponin and sarcoplasmic calcium binding proteins which were significantly affected mainly at the EC10 and EC20 dimethoate concentrations. The clear separation in expression between the lowest and highest concentrations were also observed for several transcripts related with the electron transport system, from complex I, complex III and complex IV and ATP synthase from which ultimately the energy is produced. All of these transcripts were up-regulated at lower doses and then down-regulated at higher doses, Antipyrine suggesting an inhibition of the electron transport chain and consequent ATP production with increasing concentrations. Dysfunction of the mitochondrial respiratory chain has been associated with increased peroxide and hydrogen peroxide production in cells and consequent alterations in the activity of antioxidant enzymes. Interestingly, dimethoate induced the transcript coding for the antioxidant enzyme superoxide dismutase in a concentration related manner. These transcripts with opposite expression between the lower and higher concentrations of dimethoate play an important role in the way dimethoate clustered as opposed to the way atrazine and carbendazim samples clustered. Overall, responses to the EC10 and EC20 of dimethoate are opposite from those of atrazine and carbendazim, being less distinct at EC50 and EC90. Information on mechanisms of dimethoate toxicity in other organisms is very limited and what is known is that this compound has the ability to 1) inhibit acetylcholinesterase activity in several organisms and to 2) have an influence on the metabolic pathways controlled by steroid hormones in rats. Inhibition of acetylcholinesterase activity could not be assessed from the present transcriptomic analysis since this particular transcript is not present in the library for this species. Additional work by the authors confirmed this effect, as cholinesterases activity was inhibited after 8 days of exposure. As for the second known mechanism, there are evidences in the present study pointing to an inhibition of steroidogenesis. The under-expression of sec14-like 2 transcript, involved in the positive regulation of cholesterol biosynthesis, suggests that less cholesterol will be synthesized and consequently, less steroids will be generated. Inhibition of steroidogenesis, along with the over expression of retinol dehydrogenase involved in the metabolism of vitamin A, were common mechanisms between dimethoate and atrazine toxicity. Expression of the mentioned transcripts involved in these mechanisms was further confirmed by qPCR. The role of steroids on this particular species is not known and the association of steroids with their endocrine physiology has not yet been shown.