Over-activation of the Drosophila melanogaster hsp83 gene by selenium intoxication

Abstract

Selenium is an important dietary micronutrient and an essential component of selenoproteins and the active sites of some enzymes, although at high concentrations it is toxic. We investigated diphenyl diselenide ((C 6 H 5 ) 2 Se 2 ) for its effects on the developmental stages of Drosophila melanogaster and found that in the larval and pupae stages the toxic threshold for this compound when added to the banana-agar medium on which the larva were fed was 350 μmol. In adult flies, fed on the same media, there were no observable toxic effects below 500 μmol but there were toxic effects above 600 μmol, indicating that adult flies were more resistant to selenium intoxication. In larvae, a when diphenyl diselenide was present above the toxic threshold there was increased activation of the hsp83 heat shock protein gene. Selenium promotes oxidation of sulfhydryl groups and affects the folding of proteins and this could explain the over-expression of hsp83 because the product of this gene is involved in protein folding and defense responses, including the response to heat shock.

Ovotoxicants 4-vinylcyclohexene 1,2-monoepoxide and 4-vinylcyclohexene diepoxide disrupt redox status and modify different electrophile sensitive target enzymes and genes in Drosophila melanogaster

“…The maximum average lifespan of flies used here ( D. melanogaster , Harwich strain) is about 50–58 days, and about 50% of the flies generally die within 41–45 days. However, this can vary depending on a variety of factors such as diet composition and temperature [36] .…”

Selenium and anticarcinogenesis: underlying mechanisms

“…Toxic levels of Se increased the expression of thioredoxin reductase (TRR) mRNA variants in a lung cancer cell line [15], and caused overexpression of a Drosophila heat shock protein gene for a protein-folding factor [16]. Toxic levels of Se increased the expression of thioredoxin reductase (TRR) mRNA variants in a lung cancer cell line [15], and caused overexpression of a Drosophila heat shock protein gene for a protein-folding factor [16].…”

“…3). The induction of a Drosophila heat shock protein by diphenyldiselenide appears to involve altered protein conformation associated with covalent protein-thiol disruption [16]. That Se species can act through protein-thiol modification was indicated by the finding of SeMet treatment altering the proteomic profile of redox-sensitive proteins in prostate cancer [52].…”

Low concentrations of selenium nanoparticles enhance the performance of a generalist parasitoid and its host, with no net effect on host suppression

“…There exists a delicate balance in the essential role of selenium as a micronutrient and its dosedependent toxicity in both vertebrate and invertebrate animals [40][41][42][43][44][45][52][53][54][55][56] . In insects, diets with supplemental selenium can benefit growth, survival, and reproduction, but higher concentrations can have the opposite effect 40,[43][44][45]53 .…”