Differences in the effects of sodium selenate and sodium selenite on the mortality, reproduction, lipid peroxidation and glutathione redox status of Folsomia candida Willem 1902 (Collembola)

The average selenium content of the soils worldwide is 0.4 mg kg−1; however, the selenium concentration can be much higher in some areas. Selenium is essential to humans and animals, but it can also be a risk based on the narrow gap between the beneficial and toxic concentrations. There is scarce information in the literature on the effects of various inorganic forms of selenium on soil invertebrates, such as collembolans. Consequently, the goal of our study was to determine if selenium has a negative effect on the collembolan species Folsomia candida and to verify if there is a difference between the effects of the two oxidation forms. The effect of sodium selenite and sodium selenate on Folsomia candida was studied in the laboratory by mortality and reproduction tests also by various sub-lethal and biochemical methods. The methods used in our study included a standard OECD test according to the 232 guideline, and we measured the life history parameters such as relative growth, egg production, and egg volume. For the investigation of lipid peroxidation and glutathione redox status, malondialdehyde (MDA) content, reduced glutathione (GSH) concentration and glutathione peroxidase (GPx) activity were measured. Our results showed that up to a concentration of 0.5 mg kg−1 Se in soil, both selenium forms were beneficial for F. candida. For mortality, the LOAEC (lowest observable adverse effect concentration) was 8 mg kg−1 Se in the soil in the experiments according to the OECD 232 test for both selenium forms. In case of juveniles, sodium selenite was much more toxic than sodium selenate. The LOAEC was 0.5 mg kg−1 for sodium selenite and 8 mg kg−1 in the case of sodium selenate. Sub-lethal parameters showed to be potentially more sensitive than the parameters measured in the OECD 232 test in the case of sodium selenate contamination. For instance, both the number of eggs laid and the relative growth showed significant differences compared to the control group in lower concentrations than the juvenile number or mortality. In the groups treated with sodium selenite, the juvenile number was the most sensitive parameter. Based on our results, it can be stated that sodium selenite may be potentially more toxic to collembolans than sodium selenate. Lipid peroxidation was not initiated by selenium exposure. The glutathione redox system also did not activate either, which suggested that selenium toxicity in collembola is not a consequence of selenium-induced oxidative stress.