Background
Human requirements for dietary selenium are met mainly by crops. However, excessive uptake of selenium in plants can restrict growth, and its toxicity has been postulated to target roots. Selenite toxicity can be attributed to its assimilation into selenocysteine, which can replace cysteine to yield malformed selenoproteins. Additionally, selenite has pro-oxidant properties. In this study, the effects of selenite on root tissue in Brassica napus (canola) were investigated to better understand its mode of toxicity and the metabolic adjustments needed to mediate a selenite-response.
Conclusion
Collectively, the data indicate that selenite necessitates the reconfiguration of metabolic pathways to overcome the consequences of mitochondrial oxidative stress in root tissue. Efforts to mitigate the detrimental effects of selenite-induced oxidative stress may ultimately improve selenium tolerance and accumulation in crops.
Results
Selenite induced the rapid formation of mitochondrial superoxide, which led to decreased aconitase activity and involvement of the alternative oxidase pathway. Although selenite altered primary metabolism, as observed by the increased amino acids and decreased TCA cycle metabolites, increased glucose presumably supported higher respiratory rates and ATP levels reported in this study. Additionally, evidence is presented indicating that selenite suppressed the ubiquitin-proteasome pathway, and induced the pentose phosphate pathway needed to maintain antioxidant metabolism. Selenite treatment also elevated glutathione concentration and coincided with increased levels of γ-glutamyl cyclotransferase, which may possibly degrade selenium metabolites conjugated to glutathione.