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The toxicity of compounds to cells is concentration, temperature, and exposure-time dependent.
In developing new antioxidants it will be useful to utilize endogenous processes to activate and recycle the molecules in parallel with the targeting of compounds to cells and organelles in ways that are not limited by the constraints that impair the distribution of endogenous antioxidants.
This would allow the delivery of compounds to cells on multiple occasions, without the repeated administration of drug-loaded vesicles.
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This was based on experiments adding nitric oxide and similar compounds to cell cultures of neurons and oligodendrocytes and comparing how tolerant the two kinds of cells were to toxic levels of the chemical.
Their stock solutions in DMSO were made on the day of adding each of these compounds to cell cultures.
The stock solution of LCA in water was made on the day of adding this compound to cell cultures.
Here, an additional step is included involving the addition of different concentrations of a ligand (e.g., lead compound) to cell lysates prior to processing.
The stock solution of LCA in dimethyl sulfoxide (DMSO) was made on the day of adding this compound to cell cultures.
The results of our study shed light on molecular pathways associated with the cellular response of eukaryotic cells to nickel compounds and provide potential implications for further understanding the toxic effects of nickel compounds to human cells.
This is supposedly caused by better penetration of lipophilic compounds to the cells.
This effect was similar to as shown by positive control amphotericin B. Furthermore, the binding of test compounds to yeast cells was studied by measuring the absorbance of unbound compound in supernatant (Figure 8a,b).
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