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Ze et al. [81] reported that TiO2 NPs were detected in the mouse brain after intranasal instillation.
DNA damage, determined by the comet assay, was detected in the mouse brain after mice were exposed to TiO2 NPs.
In another study, ZnO NPs inhibited the activities of SOD and GSH-Px and increased the MDA content in the mouse brain after intraperitoneal injection [77].
We find no qualitative or quantitative differences in these parameters between the transthyretin-null and the wild-type mouse brain after either [125I]thyroxine or [125I]triiodothyronine administration.
OS, determined by increased ROS production and decreased expression of CuZn-SOD and Mn-SOD, was induced in the mouse brain after administration of TiO2, ZnO, or Al2O3 NPs [76].
We have shown that the endocannabinoid 2-arachidonoyl glycerol (2-AG) is released in mouse brain after closed head injury (CHI), and treatment with exogenous 2-AG exerts neuroprotection via the central cannabinoid receptor CB1.
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We were able to identify PTAX and its metabolites in mouse brains after a cycle of 5 injections of p97-PTAX (Table 1).
Samples obtained from mouse brains after perfusion and craniotomy were cut into small fragments and immersed for 2 h in a fixative solution containing 2.5% glutaraldehyde in 0.1 M PBS, pH 7.2, at room temperature.
Compromised capillaries were found with variable frequency at different time points in Gcdh−/− mouse brains after protein diet exposure.
It remains to be determined if the survival and differentiation rates are different in adult mouse brains after IR, given the protracted inflammatory reaction.
In this study we first compared the lesion profile and extent of tissue damage in Prnp+/+ and Prnp−/− mouse brains after transient focal ischemia.
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