Assessment of genotoxicity of silver nanoparticles on lymphocyte cells of albino rats using comet assay.

Silver nanoparticles, "AgNPs", represent a prominent nanoproduct, but most of the previous toxicity studies on its genotoxicity are still limited. The current study aimed to assess the genotoxicity of AgNPs on lymphocyte cells using comet assay and to study the recovery probability. It was conducted on 50 adult male albino rats divided into "Control group", 10 rats were injected intraperitoneal, "IP", with distilled water for 28 days, and "Test groups", 40 rats were injected "IP" with 13 ± 3 nm AgNPs for 28 days, subdivided into group I: 10 rats were injected with 2 mg/kg AgNPs, group Ia: 10 rats were injected with 2 mg/kg AgNPs and left for another 4 weeks without scarification, group II: 10 rats were injected with 4 mg/kg AgNPs, and group IIa: 10 rats were injected with 4 mg/kg and left for another 4 weeks without scarification. There was a highly significant decrease in head parameters with an increase in tail parameters in both groups I and II and in group II more than group I. Moreover, there was a highly significant increase in head parameters with a decrease in tail parameters in group Ia compared with the control group and group IIa. Comets were classified according to the tail intensity and according to visual scoring for DNA damage, which revealed different grades of DNA damage with a degree of reversibility after 4 weeks stoppage of exposure. It could be concluded that AgNPs were considered to cause harmful genotoxic effects to the human body in a dose-dependent manner.

siRNA Blocking of Mammalian Target of Rapamycin (mTOR) Attenuates Pathology in Annonacin-Induced Tauopathy in Mice.

Tauopathy is a pathological hallmark of many neurodegenerative diseases. It is characterized by abnormal aggregates of pathological phosphotau and somatodendritic redistribution. One suggested strategy for treating tauopathy is to stimulate autophagy, hence, getting rid of these pathological protein aggregates. One key controller of autophagy is mTOR. Since stimulation of mTOR leads to inhibition of autophagy, inhibitors of mTOR will cause stimulation of autophagy process. In this report, tauopathy was induced in mice using annonacin. Blocking of mTOR was achieved through stereotaxic injection of siRNA against mTOR. The behavioral and immunohistochemical evaluation revealed the development of tauopathy model as proven by deterioration of behavioral performance in open field test and significant tau aggregates in annonacin-treated mice. Blocking of mTOR revealed significant clearance of tau aggregates in the injected side; however, tau expression was not affected by mTOR blockage.

Mitochondrial complex I inhibition as a possible mechanism of chlorpyrifos induced neurotoxicity.

BACKGROUND: Organophosphates (OPs) represent the most widely used class of pesticides. Although perceived as low toxicity compounds compared to the previous organochlorines, they still possess neurotoxic effects both on acute and delayed levels. Delayed neurotoxic effects of OPs include OPIDN and OPICN. The mechanisms of these delayed effects have not been totally unraveled yet. One possible contributor for neurotoxicity is mitochondrial complex I (CI) inhibition. PURPOSE: in the present study we evaluated the contributing role of (CI) inhibition in chlorpyrifos (CPF) induced delayed neuropathy in hens. METHODS: Experimented birds received 150 mg/kg of CPF, and evaluated behaviorally and biochemically. RESULTS: CPF treated hens received 150 mg/kg and developed signs of delayed neurotoxicity, which were verified by NTE inhibition. These effects were paralleled by CI inhibition and decrease in ATP level. CONCLUSIONS: The data confirms the possible role of CI inhibition in CPF induced delayed neuropathy.