Chromium is an environmental contaminant that commonly occurs in two redox forms, Cr(III) and Cr(VI), showing contrasting geochemical and ecotoxicological behaviour. Despite the consensus that Cr(VI) is more (eco)toxic than Cr(III), an increasing number of studies suggests that Cr(III) also has the potential to elicit adverse effects in biota. Understanding Cr(III) ecotoxicity using standardized laboratory tests is complicated by its peculiar chemistry that can cause a rapid decrease in exposure concentrations due to the formation of insoluble, nanoparticulate chemical species. The availability of ecotoxicological endpoints allowing a rapid evaluation of Cr(III) ecotoxicity will therefore facilitate the interpretation of experimental results. In the present study, we used the model green alga Raphidocelis subcapitata to compare the effects of Cr(III) and Cr(VI) on the activity of photosystem II (PSII) after 24 hours of exposure and those on algal growth at 72h ; i.e. the endpoint specified in the standard ISO and OECD norms. Algae (initial cell density 200,000 cell/mL) were exposed to trivalent Cr (0–0.625 mg/L) and hexavalent Cr (0–0.859 mg/L) in Erlenmeyer flasks under controlled conditions. Exposure concentrations (<0.22 µm) decreased by 50–95% (24 hours) and by 70 – 99 % (72 hours) in the case of Cr(III), but remained stable for solutions amended with Cr(VI). The inhibitory effects of Cr(VI) reached 90% for both metrics, while Cr(III) effects did not exceed 60% for algal growth and 20% for PSII inhibition. The inhibitory effect of Cr(III) on PSII after 24h was however higher than that of Cr(VI). Significant correlations between PSII inhibition at 24h and growth inhibition at 72h were observed for both Cr forms. The corresponding linear regressions (duplicate experiences) showed that a 50% inhibition in algal growth at 72h corresponded to an 11% — Cr(III) — and a 3.5–5.0% — Cr(VI) — inhibition of PSII at 24h. However, the slope of the linear regressions differed among duplicate experiences and the regressions’ intercepts were not always equal to zero (implying possible effects on growth even in the absence of effects on PSII). Additional experiences should investigate (I) the actual suitability of early PSII measurements as a proxy for growth inhibition at longer exposure times, (II) the existence of PSII vs. growth relationships for other contaminants and (III) the possibility of detecting PSII effects at shorter exposure times.
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