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The ML-( Ti 1 − X 2 + Ti X 3 + ) 3 C 2 V Al X (ML-Ti 3 C 2) crystal was exfoliated into the crystal Ti 3 C 2 MXene with coexistence of ( Ti 1 − X 2 + Ti X 3 + ) 3 C 2 V Al X MXene and Ti 2 C V Al X MXene by HF etching Ti 3 AlC 2 and ultrasonic crushing in water. Ti 3 C 2 MXene exhibits the surface plasmon effects of transverse and longitudinal surface plasmon resonance due to its surface holes and internal bound electrons. When excited by the simulated sunlight, the high energy hot holes on the surface of plasma Ti 3 C 2 MXene crystal directly oxidize the antibiotics and the organic pollutants. The electrons bound in the crystal lag behind the excitation of holes and migrate to the surface to further degradation. After 150 min of near infrared light irradiation, the degradation rates of tetracycline (TC) and ciprofloxacin (CIP) by Ti 3 C 2 MXene are 78.91% and 99.26%, respectively. They are 1.35/1.00 and 1.53/3.11 times of ML-Ti 3 C 2 and (001)TiO 2 /Ti 3 C 2. This study indicates that Ti 3 C 2 MXene has significant degradation effects on antibiotics in the full spectral range. Our work intends to provide a valuable reference for the design of the MXene full spectral photocatalyst. [Display omitted] • Ti 3 AlC 2 was exfoliated into ( Ti 1 − X 2 + Ti X 3 + ) 3 C 2 V Al X MXene and Ti 2 C V Al X MXene crystals. • Both holes and electrons on Ti 3 C 2 MXene have surface plasmon effects of TE and TM. • Electrons lag holes to form high-energy hot electrons to enhance photocatalytic activity. [ABSTRACT FROM AUTHOR]

• Food grade TiO 2 micro-/nanoparticles and SiO 2 nanoparticles can cause toxic effects to the murine intestine. • All three particles caused inflammatory damage to the intestine. • The particles altered the gut microbiota, especially mucus-associated bacteria. • Disruption of the intestinal mucus barrier and increased LPS production are key mechanisms. • Nano-TiO 2 activated the intestinal PKC/TLR4/NF-κB signalling pathway. This study aimed to compare the effects of three food-grade particles (micro-TiO 2 , nano-TiO 2 , and nano-SiO 2) on the murine intestinal tract and to investigate their potential mechanisms of action. A 28-day oral exposure murine model was established. Samples of blood, intestinal tissues and colon contents were collected for detection. The results showed that all three particles could cause inflammatory damage to the intestine, with nano-TiO 2 showing the strongest effects. Exposure also led to changes in gut microbiota, especially mucus-associated bacteria. Our results suggest that the toxic effects on the intestine were due to reduced intestinal mucus barrier function and an increase in metabolite lipopolysaccharides which activated the expression of inflammatory factors downstream. In mice exposed to nano-TiO 2 , the intestinal PKC/TLR4/NF-κB signalling pathway was activated. These findings will raise awareness of toxicities associated with the use of food-grade TiO 2 and SiO 2. [ABSTRACT FROM AUTHOR]

Manufactured zinc oxide nanoparticles (Nano-ZnO) are being used increasingly in many fields owing to their excellent physicochemical properties. Consequently, biosecurity has become a growing concern for human health and the environment. In the present study, Nano-ZnO neurotoxicity was investigated in vivo and in vitro. In vivo results showed that Nano-ZnO particles delivered through intranasal instillation were translocated to the brain, specifically deposited in the olfactory bulb, hippocampus, striatum, and cerebral cortex, and caused ultrastructural changes, oxidative damage, inflammatory responses, and histopathological damages there, which may be important for inducing Nano-ZnO neurotoxicity. Further in vitro studies on PC12 cell line illustrated that exposure to Nano-ZnO for 6 h affected cell morphology, decreased cell viability, increased lactate dehydrogenase and oxidative stress activity levels, impaired mitochondrial function, and disturbed the cell cycle. In addition, Nano-ZnO could destroy neuronal structure by affecting cytoskeleton proteins (tubulin-α, tubulin-β and NF-H), resulting in the interruption of connection between nerve cells, which lead to nervous system function damage. Meanwhile, Nano-ZnO could induce neuronal repair and regeneration disorders by affecting the growth-related protein GAP-43 and delayed neurotoxicity by affecting the calcium/calcium-regulated kinase (CAMK2A/CAMK2B protein) signaling pathway. Unlabelled Image • Nano-ZnO can be transported via the olfactory nerve pathways into the brain tissue. • Nano-ZnO can deposit in olfactory bulb, hippocampus, striatum, and cerebral cortex. • Nano-ZnO can cause toxic damage to crucial functional sub-brain regions. • Nano-ZnO can damage neuronal mitochondrial function by oxidative stress mechanism. • Nano-ZnO can reduce the expression of CAMKII, GAP43, tubulin, and NF-H in neurons. [ABSTRACT FROM AUTHOR]