Nanotechnology is expected to be promising in many fields of medical applications, mainly in cancer treatment. While a large number of very attractive exploitations open up for the clinics, regulatory agencies are very careful in admitting new nanomaterials for human use because of their potential toxicity. The very active research on new nanomaterials that are potentially useful in medicine has not been counterbalanced by an adequate knowledge of their pharmacokinetics and toxicity. The different nanocarriers used to transport and release the active molecules to the target tissues should be treated as additives, with potential side effects of themselves or by virtue of their dissolution or aggregation inside the body. Only recently has a systematic classification of nanomaterials been proposed, posing the basis for dedicated modeling at the nanoscale level. The use of in silico methods, such as nano-QSAR and PSAR, while highly desirable to expedite and rationalize the following stages of toxicological research, are not an alternative, but an introduction to mandatory experimental work.
The role of alpha-adrenoceptors in the regulation of glucose-induced insulin release (GIR) was investigated in islets of normal and neonatally streptozotocin-injected non-insulin-dependent diabetic rats (STZ). In normal islets GIR was suppressed to approximately 50% by 10(-8) M of the alpha 2-adrenergic agonist UK 14304, whereas 10(-9) M of the agonist induced a similar inhibition in STZ islets. In normal islets, suppression of GIR by UK 14304 (10(-8) M) was totally antagonized by 10(6) M idazoxan (alpha 2-antagonist) or 10(6) M phentolamine (alpha 1 + alpha 2-antagonist). In STZ islets, the inhibitory effect of UK 14304 (10(-9) M) was entirely reversed by 10(-5) M idazoxan or 10(-6) M phentolamine. The alpha 1-antagonist prazosin (10(-7)-10(-5) M) was without effect on insulin release suppressed by UK 14304 in normal and STZ islets. Insulin release at 3.3, 8.3, or 16.7 mM glucose was augmented by phentolamine but not by idazoxan. It is concluded that the inhibitory effect of catecholamines on insulin release is mediated by alpha 2-receptors in normal and STZ islets. Phentolamine augments basal and glucose-induced insulin release by a mechanism that does not involve alpha 2-adrenoceptors.
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