Interactive mode of biochar-based silicon and iron nanoparticles mitigated Cd-toxicity in maize.

Cadmium contamination poses severe environmental and health threats, necessitating effective mitigation strategies. Rice husk biochar (BC) and nanoparticle (NP) treatments are emerging strategies with limited research on their synergistic benefits. This study assesses BC, silicon NPs (nSi), and iron NPs (nFe) modifications (B-nSi, B-nFe, and B-nSi-nFe) to reduce Cd-bioavailability in soil and its toxicity in maize, not reported before. Characterization of amendments validated, nSi and nFe attachment to BC, forming new mineral crystals to adsorb Cd. We found that B-nSi-nFe induced Cd-immobilization in soil by the formation of Cd-ligand complexes with the effective retention of NPs within microporous structure of BC. B-nSi-nFe increased soil pH by 0.76 units while reducing bioavailable Cd by 49 %, than Ck-Cd. Resultantly, B-nSi-nFe reduced Cd concentrations in roots and shoots by 51 % and 75 %, respectively. Moreover, the application of B-nSi-nFe significantly enhanced plant biomass, antioxidant activities, and upregulated the expression of antioxidant genes [ZmAPX (3.28 FC), ZmCAT (3.20 FC), ZmPOD (2.58 FC), ZmSOD (3.08 FC), ZmGSH (3.17 FC), and ZmMDHAR (3.80 FC)] while downregulating Cd transporter genes [ZmNramp5 (3.65 FC), ZmHMA2 (2.92 FC), and ZmHMA3 (3.40 FC)] compared to Ck-Cd. Additionally, confocal microscopy confirmed the efficacy of B-nSi-nFe in maintaining cell integrity due to reduced oxidative stress. SEM and TEM observations revealed alleviation of Cd toxicity to stomata, guard cells, and ultracellular structures with B-nSi-nFe treatment. Overall, this study demonstrated the potential of B-nSi-nFe for reducing Cd mobility in soil-plant system, mitigating Cd-toxicity in plants and improving enzymatic activities in soil.

Ethylene accelerates copper oxide nanoparticle-induced toxicity at physiological, biochemical, and ultrastructural levels in rice seedlings.

The enormous use of metal-based nanoparticles (NPs) in different sectors may result in enhanced accumulation in agricultural soil, which could impose negative effects on crop productivity. Hence, strategies are needed to explore the mechanisms of copper oxide nanoparticle (CuO NP)-induced toxicity in crops. The present study aimed to investigate the involvement of ethylene in CuO NP-induced toxicity in rice seedlings. Here, our results indicate that 450 mg L-1 of CuO NPs induced toxic effects in rice seedlings. Thus, it was evidenced by the reduced plant biomass accumulation, enhanced oxidative stress indicators, and cellular ultrastructural damages. More importantly, the exogenous supply of ethylene biosynthesis and signaling antagonists cobalt (Co) and silver (Ag) respectively provided tolerance and improved the defense system of rice seedlings against CuO NP toxicity. The ethylene antagonists could significantly reduce the extent of ultrastructural and stomatal damage by controlling the ROS accumulation in rice seedlings under CuO NP stress. Furthermore, Co and Ag augmented the antioxidant defense system against CuO NP-induced toxicity. Contrary to that, all oxidative damage attributes were further enhanced exogenous application of ethylene biosynthesis precursor [1-aminocyclopropane-1-carboxylic acid (ACC)] in the presence of CuO NPs. In addition, ACC could increase the CuO NP-induced stomatal and ultrastructural damages by reducing the ROS-scavenging ability in rice seedlings. Taken together, these results indicate the involvement of ethylene in CuO NP-induced toxicity in rice seedlings.

Overexpression of constitutively active MAP3K7 in ameloblasts causes enamel defects of mouse teeth.

OBJECTIVE: Compelling evidence suggests that mitogen-activated protein kinases (Mapks) play an important role in amelogenesis. However, the role of transforming growth factor (TGF)-ß-activating kinase 1 (Tak1, Map3k7), which is a known upstream kinase of Mapks, during amelogenesis remains to be determined. The aim of this study was to investigate the possible involvement of Map3k7 in amelogenesis. DESIGN: We generated transgenic mice that produced constitutively active human MAP3K7 (caMAP3K7) under the control of amelogenin (Amelx) gene promoter. Radiography and micro-computed tomography (µCT) analysis was used to detect the radio-opacity and density of the teeth. The enamel microstructure was observed with a scanning electron microscope. Histological analysis was used to observe the adhesion between ameloblasts and residual organic matrix of the enamel. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to analyze the expression of enamel matrix protein. RESULTS: The enamel of mandibular molars in caMAP3K7-overexpressing mice displayed pigmentation and a highly irregular structure compared with the wild type littermates. Teeth of transgenic animals underwent rapid attrition due to the brittleness of the enamel layer. The microstructure of enamel, normally a highly ordered arrangement of hydroxyapatite crystals, was completely disorganized. The gross histological appearances of ameloblasts and supporting cellular structures, as well as the expression of the enamel protein amelotin (Amtn) were altered by the overexpression of caMAP3K7. CONCLUSIONS: Our data demonstrated that protein expression, processing and secretion occurred abnormally in transgenic mice overexpressing caMAP3K7. The overexpression of caMAP3K7 had a profound effect on enamel structure by disrupting the orderly growth of enamel prisms.