Unravelling the Polytoxicology of Chlorfenapyr on Non-Target HepG2 Cells: The Involvement of Mitochondria-Mediated Programmed Cell Death and DNA Damage.

Chlorfenapyr (CHL) is a type of insecticide with a wide range of insecticidal activities and unique targets. The extensive use of pesticides has caused an increase in potential risks to the environment and human health. However, the potential toxicity of CHL and its mechanisms of action on humans remain unclear. Therefore, human liver cells (HepG2) were used to investigate the cytotoxic effect and mechanism of toxicity of CHL at the cellular level. The results showed that CHL induced cellular toxicity in HepG2 cells and induced mitochondrial damage associated with reactive oxygen species (ROS) accumulation and mitochondrial calcium overload, ultimately leading to apoptosis and autophagy in HepG2 cells. Typical apoptotic changes occurred, including a decline in the mitochondrial membrane potential, the promotion of Bax/Bcl-2 expression causing the release of cyt-c into the cytosol, the activation of cas-9/-3, and the cleavage of PARP. The autophagic effects included the formation of autophagic vacuoles, accumulation of Beclin-1, transformation of LC3-II, and downregulation of p62. Additionally, DNA damage and cell cycle arrest were detected in CHL-treated cells. These results show that CHL induced cytotoxicity associated with mitochondria-mediated programmed cell death (PCD) and DNA damage in HepG2 cells.

Bacteriostatic effects of high-intensity ultrasonic treatment on Bacillus subtilis vegetative cells.

The bacteriostatic effects of high-intensity ultrasonic treatment (HIU) on Bacillus subtilis vegetative cells were evaluated, and the related mechanisms were explored using quantitative proteomics. The bacteriostatic effect of HIU on B. subtilis was proportional to the ultrasound treatment time and power, and the number of cultivable B. subtilis cells was decreased by approximately one log (at 270 W for 15 min) or half log (at 90 W for 25 min or 360 W for 5 min). Scanning electron microscopy images and gel electrophoresis results showed that HIU caused the destruction of the cell structure and intracellular protein leakage. In addition, HIU treatment at 270 W for 15 min resulted in the greatest decrease (84.22%) in intracellular adenosine triphosphate (ATP) content. The quantitative proteomic analysis showed that B. subtilis resisted the stress of HIU treatment by regulating the key proteins in physiological activities related to membrane transport (ATP-binding cassette [ABC] transporter), signal transduction (the two-component system), and energy metabolism (the tricarboxylic acid [TCA] cycle). HIU-induced physical damage, stress, and metabolic disorders were the main causes of the bacteriostatic effects on B. subtilis. These findings provide a foundation for the subsequent optimization and potential applications of HIU inactivation of B. subtilis.

Isochamaejasmin induces toxic effects on Helicoverpa zea via DNA damage and mitochondria-associated apoptosis.

BACKGROUND: Stellera chamaejasme L. is a poisonous plant with rich resources and is thus highly valuable in terms of new pesticide development. Isochamaejasmin (ICM), one of the main ingredients in S. chamaejasme has drawn much attention owing to its antitumour properties. However, the toxicity and mode of action of ICM on insects are still not clear. In this article, the larva and neuronal cell (AW1) of Helicoverpa zea were used to clarify the insecticidal activity of ICM as well as its toxic mechanism at the cellular level. RESULTS: The results confirmed that ICM has potential toxicity against H. zea both in vivo and in vitro via time- and dose-dependent manners. Moreover, we found that ICM caused DNA damage and increased the levels of γH2AX and OGG1 in AW1 cells. Results also showed decline in the mitochondrial membrane potential (MMP), upregulation of Bax/Bcl-2 expression resulting in the release of cytochrome c into the cytosol, activation of caspase-3/9, and cleavage of poly ADP-ribose polymerase (PARP) as a result of exposure to ICM. Additionally, a dose-dependent rise in the reactive oxygen species (ROS) levels, accumulation of a lipid peroxidation product, and inactivation of antioxidant enzymes were found in ICM-treated cells. CONCLUSION: These findings confirmed the insecticidal activity of ICM. Furthermore, the results revealed that ICM could cause DNA damage and induce apoptosis via the mitochondrial pathway in AW1 cells. This study provides the basic information needed to understand the toxicity and mechanisms of action of ICM, which could potentially be used to develop it as a new insecticide.

Investigation of novel pyrazole carboxamides as new apoptosis inducers on neuronal cells in Helicoverpa zea.

Novel pyrazole carboxamides with a diarylamine-modified scaffold were modified based on the bixafen (Bayer) fungicide, which has excellent activity against Rhizoctonia solani, Rhizoctonia cerealis and Sclerotinia sclerotiorum. To discover the potential insecticidal activity of these novel pyrazole carboxamides, the present study explored their possible cytoactivity on the insect neuronal cells (RP-HzVNC-AW1) in Helicoverpa zea. The preliminary bioassays showed that some of the target compounds exhibited good cytoactivity against AW1 cells. Among them, compounds a5 and b4-b7 showed good activity in vitro with IC50 values of 11.28, 10.46, 9.04, 11.72 and 12.19 µM, respectively. Notably, the IC50 value of compound b5 was better than 11.81 µM for fipronil. We subsequently attempted to illustrate the mechanism of b5. Intracellular biochemical assays showed that b5 induced AW1 cell apoptosis with a decrease in themitochondrial membrane potential, as well as a significantly increased intracellular calcium ion concentration and caspase-3 activity. A significant decrease in Bcl-2 levels and a marked augmentation of cytochrome-c and Bax were also detected. These results indicate that a mitochondrially dependent intrinsic pathway contributes to compound b5-induced apoptosis in AW1 cells. This study suggests that b5 may act as a potential insecticide that can be used for further optimization.

Highly Dispersed Nickel-Containing Mesoporous Silica with Superior Stability in Carbon Dioxide Reforming of Methane: The Effect of Anchoring.

A series of nickel-containing mesoporous silica samples (Ni-SiO2) with different nickel content (3.1%-13.2%) were synthesized by the evaporation-induced self-assembly method. Their catalytic activity was tested in carbon dioxide reforming of methane. The characterization results revealed that the catalysts, e.g., 6.7%Ni-SiO2, with highly dispersed small nickel particles, exhibited excellent catalytic activity and long-term stability. The metallic nickel particle size was significantly affected by the metal anchoring effect between metallic nickel particles and unreduced nickel ions in the silica matrix. A strong anchoring effect was suggested to account for the remaining of small Ni particle size and the improved catalytic performance.

Two Dawson-templated three-dimensional metal-organic frameworks based on oxalate-bridged binuclear cobalt(II)/Nickel(II) SBUs and Bpy linkers.

The Dawson anion P 2W 18O 62 (6-) has been used as a noncoordinating polyoxoanion template for the construction of two metal-organic frameworks, namely, [M 2(bpy) 3(H 2O) 2(ox)][P 2W 18O 62]2(H 2-bpy). nH 2O (M = Co(II), n = 3 ( 1); M = Ni(II), n = 2 ( 2)) (bpy = 4,4'-bipyridine; ox = C 2O 4 (2-)). Single-crystal X-ray analysis reveals that both of the structures exhibit 3D host frameworks constructed from the oxalate-bridged binuclear superoctahedron secondary building units (SBUs) and bpy linkers and the voids of which are occupied by Dawson anions, guest bpy, and water molecules. Magnetic studies reveal that there are antiferromagnetic exchange interactions among the transition-metal centers in compounds 1 and 2. Furthermore, a compound 1-modified carbon paste electrode ( 1-CPE) displays good electrocatalytic activity toward the reduction of nitrite.