Different functional groups of carbon dots influence the formation of protein crowns and pepsin characteristic in vitro digestion.

Application of nanomaterials (NMs) in agriculture poses an ingestion risk to humans and may affect the digestive process. Different fates of NMs with differential charges in the gastrointestinal tract should be considered. In this study, the interaction between three carbon dots (CDs) carried with different functional groups (-NH2, -OH, and -COOH) and pepsin was analyzed through an in vitro digestion model. The results showed that CDs significantly reduced pepsin activity. Among them, CDs-NH2 had the greatest effect, following by CDs-OH, and CDs-COOH. Besides, molecular docking demonstrated the specific binding site of CDs to pepsin, while the most stable binding energy (-8.10 kcal/mol) was formed between CDs-NH2 and pepsin. Further, CDs formed a nanomaterial-protein crown structure with pepsin. The present study enriches the functional group properties of CDs in the digestion and provides new ideas for the potential human health of NMs.

Nanoplastic impacts on the foliar uptake, metabolism and phytotoxicity of phthalate esters in corn (Zea mays L.) plants.

Nanoplastic pollution in terrestrial plants is of increasing concern for its negative effects on living organisms. However, the impacts of nanoplastics on chemical processes and plant physiology of phthalate esters (PAEs) remain unclear. The present work offers insight into the foliar uptake, metabolism and phytotoxicity of two typical PAEs, namely, di-n-butyl phthalate (DBP) and di-(2-ethylhexyl) phthalate (DEHP), in corn (Zea mays L.) seedlings and the effects of amino-functionalized polystyrene nanoplastics (PSNPs-NH2). The presence of PSNPs-NH2 increased DBP and DEHP accumulation in the leaves by 1.36 and 1.32 times, respectively. PSNPs-NH2 also promoted the leaf-to-root translocation of DBP and DEHP, with the translocation factor increasing by approximately 1.05- and 1.16-fold, respectively. Furthermore, the addition of PSNPs-NH2 significantly enhanced the transformation of PAEs to their primary metabolites, mono-butyl phthalate and mono(2-ethylhexyl) phthalate in corn leaves and roots. The co-presence of PSNPs-NH2 and PAEs showed stronger impairment of photosystem II efficiency via the downregulation of transporter D1 protein, thus exhibiting a greater inhibitory effect on plant growth. Our findings reveal that nanoplastics promote the foliar uptake and transformation of PAE chemicals in crops and exacerbate their toxicity to crop plants, thereby threatening agricultural safety and human health.

Foliar uptake and leaf-to-root translocation of nanoplastics with different coating charge in maize plants.

Foliar uptake of nanoplastics could represent a pathway responsible for pollutant loads in crop plants, thereby posing risks to human health. To evaluate the foliar uptake, leaf-to-root translocation of nanoplastics, as well as the influences of surface charge on the above processes and physiological effects to plants, maize (Zea mays L.) seedlings were foliar exposed to carboxyl-modified polystyrene nanoplastics (PS-COOH) and amino-modified polystyrene nanoplastics (PS-NH2), respectively. Both PS nanoplastics could effectively accumulate on the maize leaves, accompanied by observable particle aggregation. Due to electrostatic attraction to the negatively charged cell wall, positively charged PS-NH2 association with the leaf surfaces was significantly more than negatively charged PS-COOH. The fraction of PS nanoplastics entry into the leaves could efficiently transfer to the vasculature mainly through stomatal opening and move down to the roots through vascular bundle. Meanwhile, the occurrence of aggregation limited the nanoplastic translocation to the roots, especially for PS-NH2 with larger aggregate sizes relative to PS-COOH. Compared with negatively charged PS-COOH, positively charged PS-NH2 treatment had a higher inhibitory effect on photosynthesis and a stronger stimulation to the activity of antioxidant systems. Overall, our findings give a scientific basis for the risk assessment of nanoplastic exposure in air-plant systems.

Cell wall: An important medium regulating the aggregation of quantum dots in maize (Zea mays L.) seedlings.

Quantum dots (QDs) find various applications in many fields, leading to increasing concerns regarding their uptake and subsequent interaction with plant body. Cell wall (CW), serving as a first target place that interacts with xenobiotic substances into plant body, its role in regulating the QDs cellular uptake needs to be explored. In the present study, maize (Zea mays L.) seedlings were hydroponically exposed to PEG-COOH-CdS/ZnS QDs (QDs-PEG-COOH) and MPA-CdS/ZnS QDs (QDs-MPA) functionalized with negatively charged and neutral coatings, respectively. Uptake rate of QDs-PEG-COOH was approximately 3.5 times lower than that of QDs-MPA due to electrostatic repulsion to the negatively charged root CW. Both types of QDs had obvious aggregation on surfaces of taproot, lateral root and fibrous root, and QDs-MPA aggregates were approximately 1.8 times larger than QDs-PEG-COOH aggregates. The strong hydrogen bond formed by hydroxyl group in cellulose of CW and carboxyl group on surface coatings of QDs-PEG-COOH constituted the key mechanism for QDs-PEG-COOH aggregation, while conjugated CË­C chains between lignin and QDs-MPA dominated the occurrences of QDs-MPA aggregation. Results of this work highlight the importance of plant CW in regulating uptake rate and aggregation of QDs, potentially limiting their internalization into plant body and introduction into food webs.

Interaction of leptin and amylin in the long-term maintenance of weight loss in diet-induced obese rats.

We have previously shown that combined amylin + leptin agonism elicits synergistic weight loss in diet-induced obese (DIO) rats. Here, we assessed the comparative efficacy of amylin, leptin, or amylin + leptin in the maintenance of amylin + leptin-mediated weight loss. DIO rats pretreated with the combination of rat amylin (50 microg/kg/day) and murine leptin (125 microg/kg/day) for 4 weeks were subsequently infused with either vehicle, amylin, leptin, or amylin + leptin for an additional 4 weeks. Food intake, body weight, body composition, plasma parameters, and the expression of key metabolic genes in liver and white adipose tissue (WAT) were assessed. Amylin + leptin treatment (weeks 0-4) reduced body weight to 87.5% of baseline. Rats subsequently maintained on vehicle or leptin regained all weight (to 104.2 and 101.2% of baseline, respectively), those maintained on amylin had partial weight regain (97.0%). By contrast, weight loss was largely maintained with continued amylin + leptin treatment (91.4%), associated with a 10% decrease in adiposity. Cumulative food intake (weeks 5-8) was reduced by amylin and amylin + leptin, but not by leptin alone. Amylin + leptin, but not amylin or leptin alone, reduced plasma triglycerides (by 55%), total cholesterol (by 19%), and insulin (by 57%) compared to vehicle. Amylin + leptin also reduced hepatic stearoyl-CoA desaturase-1 (Scd1) mRNA, and increased WAT mRNA levels of adiponectin, fatty acid synthase (Fasn), and lipoprotein lipase (Lpl). We conclude that, in DIO rats, maintenance of amylin + leptin-mediated weight loss requires continued treatment with both agonists, and is accompanied by sustained improvements in body composition, and indices of lipid metabolism and insulin sensitivity.

Amylin-mediated restoration of leptin responsiveness in diet-induced obesity: magnitude and mechanisms.

Previously, we reported that combination treatment with rat amylin (100 microg/kg.d) and murine leptin (500 microg/kg.d) elicited greater inhibition of food intake and greater body weight loss in diet-induced obese rats than predicted by the sum of the monotherapy conditions, a finding consistent with amylin-induced restoration of leptin responsiveness. In the present study, a 3 x 4 factorial design was used to formally test for a synergistic interaction, using lower dose ranges of amylin (0, 10, and 50 microg/kg.d) and leptin (0, 5, 25, and 125 microg/kg.d), on food intake and body weight after 4 wk continuous infusion. Response surface methodology analysis revealed significant synergistic anorexigenic (P < 0.05) and body weight-lowering (P < 0.05) effects of amylin/leptin combination treatment, with up to 15% weight loss at doses considerably lower than previously reported. Pair-feeding (PF) experiments demonstrated that reduction of food intake was the predominant mechanism for amylin/leptin-mediated weight loss. However, fat loss was 2-fold greater in amylin/leptin-treated rats than PF controls. Furthermore, amylin/leptin-mediated weight loss was not accompanied by the counterregulatory decrease in energy expenditure and chronic shift toward carbohydrate (rather than fat) utilization observed with PF. Hepatic gene expression analyses revealed that 28 d treatment with amylin/leptin (but not PF) was associated with reduced expression of genes involved in hepatic lipogenesis (Scd1 and Fasn mRNA) and increased expression of genes involved in lipid utilization (Pck1 mRNA). We conclude that amylin/leptin interact synergistically to reduce body weight and adiposity in diet-induced obese rodents through a number of anorexigenic and metabolic effects.

PYY[3-36] administration decreases the respiratory quotient and reduces adiposity in diet-induced obese mice.

In rodents, weight reduction after peptide YY[3-36] (PYY[3-36]) administration may be due largely to decreased food consumption. Effects on other processes affecting energy balance (energy expenditure, fuel partitioning, gut nutrient uptake) remain poorly understood. We examined whether s.c. infusion of 1 mg/(kg x d) PYY[3-36] (for up to 7 d) increased metabolic rate, fat combustion, and/or fecal energy loss in obese mice fed a high-fat diet. PYY[3-36] transiently reduced food intake (e.g., 25-43% lower at d 2 relative to pretreatment baseline) and decreased body weight (e.g., 9-10% reduction at d 2 vs. baseline) in 3 separate studies. Mass-specific metabolic rate in kJ/(kg x h) in PYY[3-36]-treated mice did not differ from controls. The dark cycle respiratory quotient (RQ) was transiently decreased. On d 2, it was 0.747 +/- 0.008 compared with 0.786 +/- 0.004 for controls (P < 0.001); light cycle RQ was reduced throughout the study in PYY[3-36]-treated mice (0.730 +/- 0.006) compared with controls (0.750 +/- 0.009; P < 0.001). Epididymal fat pad weight in PYY[3-36]-treated mice was approximately 50% lower than in controls (P < 0.01). Fat pad lipolysis ex vivo was not stimulated by PYY[3-36]. PYY[3-36] decreased basal gallbladder emptying in nonobese mice. Fecal energy loss was negligible ( approximately 2% of ingested energy) and did not differ between PYY[3-36]-treated mice and controls. Thus, negative energy balance after PYY[3-36] administration in diet-induced obese mice results from reduced food intake with a relative maintenance of mass-specific energy expenditure. Fat loss and reduced RQ highlight the potential for PYY[3-36] to drive increased mobilization of fat stores to help meet energy requirements in this model.