The constant evolution and applications of metallic nanoparticles (NPs) make living organisms more susceptible to being exposed to them. Among the most used are zinc oxide nanoparticles (ZnO-NPs). Therefore, understanding the molecular effects of ZnO-NPs in biological systems is extremely important. This review compiles the main mechanisms that induce cell toxicity by exposure to ZnO-NPs and reported in vitro research models, with special attention to mitochondrial damage. Scientific evidence indicates that in vitro ZnO-NPs have a cytotoxic effect that depends on the size, shape and method of synthesis of ZnO-NPs, as well as the function of the cells to which they are exposed. ZnO-NPs come into contact with the extracellular region, leading to an increase in intracellular [Zn²⁺] levels. The mechanism by which intracellular ZnO-NPs come into contact with organelles such as mitochondria is still unclear. The mitochondrion is a unique organelle considered the “power station” in the cells, participates in numerous cellular processes, such as cell survival/death, multiple biochemical and metabolic processes, and holds genetic material. ZnO-NPs increase intracellular levels of reactive oxygen species (ROS) and, in particular, superoxide levels; they also decrease mitochondrial membrane potential (MMP), which affects membrane permeability and leads to cell death. ZnO-NPs also induced cell death through caspases, which involve the intrinsic apoptotic pathway. The expression of pro-apoptotic genes after exposure to ZnO-NPs can be affected by multiple factors, including the size and morphology of the NPs, the type of cell exposed (healthy or tumor), stage of development (embryonic or differentiated), energy demand, exposure time and, no less relevant, the dose. To prevent the release of pro-apoptotic proteins, the damaged mitochondrion is eliminated by mitophagy. To replace those mitochondria that underwent mitophagy, the processes of mitochondrial biogenesis ensure the maintenance of adequate levels of ATP and cellular homeostasis.

Canine distemper is caused by canine distemper virus (CDV), a multisystemic infectious disease with a high morbidity and mortality rate in dogs. Nanotechnology represents a development opportunity for new molecules with antiviral effects that may become effective treatments in veterinary medicine. This study evaluated the efficacy and safety of silver nanoparticles (AgNPs) in 207 CDV, naturally infected, mixed-breed dogs exhibiting clinical signs of the non-neurological and neurological phases of the disease. Group 1a included 52 dogs (experimental group) diagnosed with non-neurologic distemper treated with 3% oral and nasal AgNPs in addition to supportive therapy. Group 1b included 46 dogs (control group) diagnosed with non-neurological distemper treated with supportive therapy only. Group 2a included 58 dogs with clinical signs of neurological distemper treated with 3% oral and nasal AgNPs in addition to supportive therapy. Group 2b included 51 dogs (control group) diagnosed with clinical signs of neurological distemper treated with supportive therapy only. Efficacy was measured by the difference in survival rates: in Group 1a, the survival rate was 44/52 (84.6%), versus 7/46 in Group 1b (15.2%), while both showed clinical signs of non-neurological distemper. The survival rate of dogs with clinical signs of neurological distemper in Group 2a (38/58; 65.6%) was significantly higher than those in Control Group 2b (0/51; 0%). No adverse reactions were detected in experimental groups treated with AgNPs. AgNPs significantly improved survival in dogs with clinical signs of neurological and non-neurological distemper. The use of AgNPs in the treatment of neurological distemper led to a drastic increase in the proportion of dogs recovered without sequels compared to dogs treated without AgNPs. The evidence demonstrates that AgNP therapy can be considered as a targeted treatment in dogs severely affected by canine distemper virus.

The dermoid cyst considered a cystic teratoma derived from embryonic germinal epithelium is a slow-growing benign tumour. Dermoid cysts may occur in the orbital and periorbital region in paediatric patients and are often recurrent. The surgical approach depends upon the site of the lesion, superficial or deep. To our knowledge, this is the first described case of a patient with resection of dermoid cyst treated with human amniotic membrane implant and topical application of 0.02% mitomycin C. We present a case of a 12-year-old male with a tumour in the superotemporal region of the right eye (RE). Symptoms included decreased visual acuity (VA), burning eye, foreign body sensation, and photophobia of the affected eye. A physical examination detected blepharospasm. Ophthalmic examination of his RE, fingers count from a 1–2 m distance, showed no improvement with pinhole. Visual acuity was 20/20 on the left eye (LE). The bio-microscopic examination confirmed the presence of a tumour mass (15 mm × 12 mm) on the surface of the RE, invading the superotemporal sector. The tumour had a lobulated appearance, a shiny and vascularized surface covered by conjunctiva, a pearlescent-pink colour, a medium consistency, was renitent and painless. An ultrasound scan revealed atrophy of the pigmented retinal epithelium with scleral indentation of the RE. A computed tomography (CT) scan revealed a recurrent lesion consistent with an epibulbar dermoid cyst. Surgical excision of the lesion was performed and a human amniotic membrane (HAM) graft and topical 0.02% mitomycin C (MMC) were applied. Histopathological analysis confirmed the diagnosis of recurrent dermoid cyst. In this case report, we describe a case of recurrent epibulbar dermoid cyst treated with complete resection; topical MMC and HAM implant with good clinical outcome of the lesion and implant adhesion. Resection of a cyst of the ocular surface is not recommended when a large epibulbar dermoid tissue needs to be resected and no HAM graft is available.