Nanomaterials have gained a rapid increase in use in a variety of applications that pertain to many aspects of human life. The majority of these innovations are centered on medical applications and a range of industrial and environmental uses ranging from electronics to environmental remediation. Despite the advantages of NPs, the knowledge of their toxicological behavior and their interactions with the cellular machinery that determines cell fate is extremely limited. This review is an attempt to summarize and increase our understanding of the mechanistic basis of nanomaterial interactions with the cellular machinery that governs cell fate and activity. We review the mechanisms of NP-induced necrosis, apoptosis and autophagy and potential implications of these pathways in nanomaterial-induced outcomes. Abbreviations: Ag, silver; CdTe, cadmium telluride; CNTs, carbon nanotubes; EC, endothelial cell; GFP, green fluorescent protein; GO, graphene oxide; GSH, glutathione; HUVECs, human umbilical vein endothelial cells; NP, nanoparticle; PEI, polyethylenimine; PVP, polyvinylpyrrolidone; QD, quantum dot; ROS, reactive oxygen species; SiO, silicon dioxide; SPIONs, superparamagnetic iron oxide nanoparticles; SWCNT, single-walled carbon nanotubes; TiO, titanium dioxide; USPION, ultra-small super paramagnetic iron oxide; ZnO, zinc oxide.

Diabetic neuropathy (DN) is a widespread disabling disorder comprising peripheral nerves' damage. DN develops on a background of hyperglycemia and an entangled metabolic imbalance, mainly oxidative stress. The majority of related pathways like polyol, advanced glycation end products, poly-ADP-ribose polymerase, hexosamine, and protein kinase c all originated from initial oxidative stress. To date, no absolute cure for DN has been defined; although some drugs are conventionally used, much more can be found if all pathophysiological links with oxidative stress would be taken into account. In this paper, although current therapies for DN have been reviewed, we have mainly focused on the links between DN and oxidative stress and therapies on the horizon, such as inhibitors of protein kinase C, aldose reductase, and advanced glycation. With reference to oxidative stress and the related pathways, the following new drugs are under study such as taurine, acetyl-L-carnitine, alpha lipoic acid, protein kinase C inhibitor (ruboxistaurin), aldose reductase inhibitors (fidarestat, epalrestat, ranirestat), advanced glycation end product inhibitors (benfotiamine, aspirin, aminoguanidine), the hexosamine pathway inhibitor (benfotiamine), inhibitor of poly ADP-ribose polymerase (nicotinamide), and angiotensin-converting enzyme inhibitor (trandolapril). The development of modern drugs to treat DN is a real challenge and needs intensive long-term comparative trials.

The objective of this study was to survey aluminum phosphide (AIP) poisoning in a referral poisoning hospital in Tehran servicing an estimation of 10,000,000 populations. Records of all patients admitted and hospitalized during a period of 7 years from January 2000 to January 2007 were collected and analyzed according to gender, age, cause of intoxication, amount of AIP consumed, route of exposure, time between exposure and onset of treatment, signs and symptoms of intoxication at admission, therapeutic intervention, laboratory tests, and outcome. During the studied years, 471 patients were admitted to the hospital with AIP poisoning; 50% of them were men. The overall case fatality ratio was 31%. The mean age was 27.1 years, and most of the patients were between 20 and 40 years old. Self-poisoning was observed in 93% of cases. The average ingested dose was 5.1 g, and most of the patients (73%) consumed 1–3 tablets of AIP. A wide range of symptoms and signs was seen on admission, but the most common one was cardiovascular manifestations (78.12%). The majority (65%) of patients were from Tehran. Poisoning in spring and winter (34% and 24%, respectively) was more common than other seasons. Gastric decontamination with potassium permanganate, and administration of calcium gluconate, magnesium sulfate, sodium bicarbonate, and charcoal were considered for most of the patients. Mean arterial blood pH was 7.23 and bicarbonate concentration was 12.7 mEq/L. One-hundred percent of patients with blood pH <7 died and 100% of patients with blood pH ≥ 7.35 survived. Electrocardiogram (EKG) abnormalities were noted in 65.6% of cases. There was a significant difference between survival and non-survival according to pH, HCO3 concentration, and EKG abnormality. Even without an increase in resources, there appears to be significant opportunities for reducing mortality by better medical management and further restrictions on the AIP tablets usage. Arterial blood pH seems to be a prognostic factor for the outcome of AIP-poisoned patients.

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The combination of nanocerium and sodium selenite is more effective than either alone in improving diabetes-induced oxidative stress.