Instead, physiologically based kinetic models have gained special importance for toxicology and have been recognized as a valuable tool to explain toxicity phenomena and underlying mechanisms (Bessems et al. 2014).
This research is the first to link toxic effects directly to a THF degradation product (γ-butyrolactone) rather than to C60 and may explain toxicity attributed to C60 in other investigations.
For example, in some studies, the presence of metal trace impurities explains demonstrated toxicity and reactive oxygen species (ROS) production[50], whereas in other cases, no such effects were reported[51].
Our results provide a new model that explains the toxicity of expanded polyQ proteins, in which the interplay between polyQ regions and other aggregation-prone domains plays a key role in determining the aggregation pathway.
Thus, response addition alone explains the toxicity associated with a pesticide mixture.
Another possible mechanism to explain the toxicity of amyloid deposits is direct toxicity to cells [ 2].
However, the toxicity observed by ionic cobalt alone did not explain the toxicity of the WC-Co nanoparticles, suggesting that the combination of metallic Co and WC is the cause of the increased particle toxicity of WC-Co.
Since the IC50 of the blank particles is about 500-fold greater than the concentration required to deliver the IC50 concentration of paclitaxel (Table 1), the increased toxicity of the drug-loaded nanoparticles cannot be explained by toxicity of the nanoparticle itself.
An important question is whether we can explain the toxicity of ginkgolides in insects, and the lack of toxicity in humans.
Late genitourinary (GU) toxicity after radiation therapy limits the quality of life of prostate cancer survivors; however, efforts to explain GU toxicity using patient and dose information have remained unsuccessful.
The lower HRT in D5 (Table 2) may also explain lower toxicity.
