Suppression of low dose streptozotocin induced diabetes in mice by administration of a nitric oxide synthase inhibitor

Suppression of nitric oxide toxicity in islet cells by α‐tocopherol

“…The administration of inhibitors of NO synthases has been found to decrease or prevent tissue damage in a large number of chronic inflammatory diseases including immune complex glomerulonephritis, graft versus host disease and arthritis [3,4]. A role of NO in the pathogenesis of type I diabetes has been suggested [33,34], and the administration of large doses of c~-tocopherol prevented spontaneous autoimmune diabetes in the NOD mouse [35] while only minor effects were seen in the BB rat diabetes model [36,37]. Taken together these data imply that ~-tocopherol participates not only in the cellular oxygen radical defence system but also mediates protection from undesired NO toxicity, c~-Tocopherol thus qualifies as a member of the cellular NO defence system, when the majority of compounds remain to be identified.…”

Zinc sulphate induces metallothionein in pancreatic islets of mice and protects against diabetes induced by multiple low doses of streptozotocin

“…In vitro, NO´produced by activated macrophages destroyed beta cells [48,49]. In vivo, inhibition of NO´generation prevented diabetes induced by MLD-STZ [5,50]. Other investigators, in contrast, neither observed NO´generation in islets isolated from mice treated with MLD-STZ [51] nor prevented diabetes induced by MLD-STZ with inhibitors of NO´generation [52].…”

Efficacy of 1400 W, a novel inhibitor of inducible nitric oxide synthase, in preventing interleukin-1beta-induced suppression of pancreatic islet function in vitro and multiple low-dose streptozotocin-induced diabetes in vivo

“…For instance, it has been proposed that NO is not formed in the MLDS model (23). Moreover, in that model it has been reported that N G -monomethyl-L-arginine was effective (24), whilst N G -nitro-L-arginine was effective (25) or not effective (26) in counteracting the development of hyperglycemia, whereas aminoguanidine did not protect against hyperglycemia (27). Furthermore, iNOS knock-out mice were protected against MLDS-induced diabetes (11).…”