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Titanium dioxide nanoparticles (TiO 2 NPs) are amongst the most frequently used nanomaterial in everyday consumer products, and their widespread applications have raised concerns of the consequent deleterious effects on human health, particularly to vulnerable populations, such as lactating females remains elusive. Therefore, this study was initiated to investigate the detrimental effects and toxic mechanisms induced by TiO 2 NPs in maternal dams and offspring during the lactation period. Dams were randomly divided into three groups. The water (Control; Group I) and TiO 2 NPs (100 mg/kg; Group II) were orally administered from postnatal day 1-20, respectively. The results indicated that TiO 2 NPs could cause toxicity in the dams, such as pathological damages to mammary gland tissues. The excessive accumulation of TiO 2 NPs could induce oxidative stress in the mammary gland, leading to the dysfunctional blood-milk barrier; besides, TiO 2 NPs could also be transferred to offspring via breastfeeding, causing abnormal development of infant. We further accessed the possible underlying molecular mechanism; for this, we orally administered TiO 2 NPs with vitamin E (100 mg/kg; Group III). The results revealed that toxicity induced by TiO 2 NPs was rescued. Collectively, this study presented the deleterious pathological effects of oral exposure to TiO 2 NPs in the mammary gland tissues and blood-milk barrier via the production of reactive oxygen species (ROS) in dams and developmental concerns in offspring. However, the administration of VE could mitigate the toxic effects induced by the TiO 2 NPs., (Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.)

Human were given a lot of opportunities to ingest TiO 2 NPs in the environment. Children have low, sensitive intestinal tolerance, and they could be exposed to higher levels of TiO 2 NPs than adults. Few studies have been conducted on the interaction between TiO 2 NPs and juvenile intestine phase models. Thus, in this work, weaning rats were orally exposed to TiO 2 NPs for 7 and 14 days. Results indicate that Ti accumulated in the intestine, liver, and feces. Inflammatory infiltration damage was observed in the colonic epithelial tissue, and gut microbiota fluctuated with a decreased abundance of Lactobacilli in feces. Oral supplementation with Lactobacillus rhamnosus GG (LGG) lessened TiO 2 NPs-induced colonic inflammatory injury, which might due to downregulation of nuclear factor kappa-B (NF-κB). Meanwhile, LGG maintained normal intestinal microbiome homeostasis, thereby improving TiO 2 NPs-induced colon injury in juvenile rats. Moreover, fecal microbiota transplant (FMT) experiment indicated possible TiO 2 NPs-induced intestinal microbiota disorder led to colonic inflammation. Our works suggested the urgent need for additional studies on the risk safety assessment, mechanism, and prevention of juvenile health damage from exposure to TiO 2 NPs., (Copyright © 2020 Elsevier Inc. All rights reserved.)