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Gene expression in rats fed 2 and 5 μg Se/g diet was compared with Se adequate rats (0.24 μg Se/g diet).
The selenoenzyme glutathione peroxidase-1 (Gpx1) is highly regulated by dietary Se, decreasing in Se deficiency to < 1% of Se adequate levels in Se-deficient liver [ 1].
This outcome might be explained by the fact that puretone thresholds at 4 kHz are typically not per se adequate predictors of speech reception threshold, unless they are combined with thresholds at lower frequencies, at 2 kHz or lower [ 50].
In rat study 1, liver Se increased to a plateau at 0.08 μg Se/g diet, remained at this level until 0.24 μg Se/g diet, and then increased gradually to 180% of Se adequate levels in rats fed 0.8 μg Se/g diet [ 8].
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Plasma Gpx3 activity in Se-deficient mice dropped to 13% of Se-adequate levels.
No genes were significantly up-regulated in Se-deficient kidney as compared to Se-adequate kidney (Table 1).
A decrease in liver Gpx1 activity to 77% of Se-adequate levels was observed in rats fed 5 μg Se/g diet, similar to previous results [ 1].
Thus, the Se-deficient animals were Se-deficient at the biochemical and molecular level, but otherwise indistinguishable from Se-adequate animals.
Most notable of the regulated selenoprotein genes is Gpx1, with its expression dropping to < 10% of Se-adequate levels in the rat model.
Liver Se and Gpx activities in mice fed the Se-marginal diet (0.05 μg Se/g diet) were intermediate between Se-deficient and Se-adequate mice.
In contrast, Se intakes less than 5 μg Se/g diet significantly changed < 10 transcripts as compared to a <span class="lh lhl">Se-adequate intake within an experiment.
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