Almond hull, a substantial byproduct constituting more than half of almond fresh weight, has garnered recent attention due to its abundance in fiber and bioactive content. Despite this huge interest, data on its toxicity remain scarce. In line with the Organization for Economic Cooperation and Development (OECD) 423 guidelines, this study conducted an acute oral toxicity test using almond hull powders processed from three major almond varieties of Butte, Monterey, and Nonpareil on BALB/c female mice, administering dosages of 300 mg/kg body weight (bw), 2000 mg/kg bw, and 5000 mg/kg bw, with observations over a 14-day period. The results indicated that almond hull powders were non-toxic, aligning with the Globally Harmonized System’s classification. Administering up to 5000 mg/kg bw of all three varieties of almond hull powders (female BALB/c mice) and 10,000 mg/kg bw of Monterey almond hull powders (both female and male mice) induced no adverse effects in terms of mortality, body weight changes, food intake, organ to weight ratio, and clinical biochemistry. Additionally, histopathological examination revealed no organ abnormalities. This study demonstrates the non-toxic nature of almond hull as an edible food ingredient under experimental conditions, encouraging the further exploration of its potential for safe consumption and its health benefits.

Almond hull, a substantial byproduct comprising more than half of almond fresh weight, has recently gained attention due to its functionality and sustainability benefits. Despite heightened interest, information regarding its toxicity remains limited. In order to assess its genotoxic potential, we conducted Good Laboratory Practice-compliant in vitro and in vivo studies following Organization for Economic Co-operation and Development (OECD) guidelines. No evidence of toxicity or mutagenicity was observed in a bacterial reverse mutation assay using five tester strains, evaluating almond hull at concentrations up to 5 mg/plate, with or without metabolic activation. Almond hull did not induce chromosome structural damage in a chromosome aberration assay using Chinese hamster ovary cells, nor did it cause any spermatogonial chromosomal aberration in tested male BALB/c mice. To evaluate its ability to induce DNA damage in rodents, a combined micronucleus assay was conducted in KM mice of both sexes. Almond hull was administered at doses of 1250, 2500, and 5000 mg/kg/day via gavage once daily for 2 days. No adverse effects of almond hull were observed in the micronucleus assay. Our results indicate no evidence of the genotoxic potential of almond hull administered up to the maximum concentrations of 5 g/kg, as recommended by OECD guidelines.

The advancement of modern lifestyles has precipitated excessive consumption of energy-dense foods, driving the escalating global burden of lipid metabolism dysregulation-related pathologies—including obesity, type 2 diabetes mellitus (T2DM), non-alcoholic fatty liver disease (NAFLD), and cardiovascular disorders—which collectively pose a formidable challenge to global public health systems. The almond hull, as a by-product of almond processing, is rich in polyphenolic compounds with demonstrated antioxidant, anti-inflammatory, and lipid-lowering potential, though its precise hypo-lipidemic mechanisms remain elusive. In this study, polyphenols were extracted from almond hulls using 50% ethanol with ultrasound-assisted extraction, followed by preliminary purification via solvent partitioning. The ethyl acetate fraction was analyzed by liquid chromatography–mass spectrometry (LC-MS). Network pharmacology and molecular docking were employed to investigate the interactions between key bioactive constituents (e.g., quercetin, baicalein, and kaempferol) and targets in lipid metabolism-related pathways. Molecular dynamics (MD) simulations further evaluated the stability of the lowest-energy complexes. Results revealed that the ethyl acetate fraction exhibited potent pancreatic lipase inhibitory activity (IC50 = 204.2 µg/mL). At 0.1 mg/mL after 24 h treatment, it significantly reduced free fatty acids (FFAs)-induced intracellular triglyceride accumulation (p < 0.01) and enhanced cellular antioxidant capacity. Network pharmacology and in vitro studies suggest almond hull extract modulates PI3K-AKT signaling and improves insulin resistance, demonstrating lipid-lowering effects. These findings support its potential in functional foods and pharmaceuticals, though further in vivo validation and mechanistic investigations are required.

This study evaluated strategies for preventing biofilm formation on stainless steel sensor mesh screens by integrating anti-fouling approaches and applying mathematical models to stimulate biofilm elimination during anti-fouling processes. Results showed that the proposed sensor mesh housing equipped with an external low-level strength electric field effectively reduced microbial biofilm formation and mitigated sensor mesh biofouling. Additionally, the combined application of the alternating electric field and ultrasonic irradiation significantly enhanced biofilm prevention and control. Anti-fouling tests conducted in natural lake water revealed that microalgae and bacteria can form biofilms on stainless steel screen electrodes in a time-dependent manner, with the 48-h time interval being crucial for cell adhesion and biofilm formation. Moreover, the dynamic process of biofilm elimination during ultrasonic treatment was successfully simulated using different mathematic models, demonstrating their suitability for describing these anti-fouling processes. This work provides valuable insights into the protection of water-monitoring sensors and probes, and to minimize biofouling through the combined use of stainless steel mesh, electric field, and ultrasonic irradiation to ensure long-term performance of sensors in aquatic high-fouling environments.

Bactericidal and bacteriostatic efficacy of light irradiation, e.g. intense pulsed light (IPL), is mainly derived from the disrupting effects of photoenergy on bacterial biomolecules, including genes, proteins, and metabolites. Previous studies have revealed the effects of IPL on genes and proteins. However, little is known about the influences of IPL on bacterial metabolism. In this study, E. coli K‐12 was treated by the IPL for 0‐20 s. Time‐ and dose‐dependent decrease of colony‐forming units and morphological changes were observed. The IPL‐induced changes in the bacterial metabolome were characterized by the liquid chromatography‐mass spectrometry‐based metabolomic analysis of membrane and cytoplasmic metabolites. The results from multivariate modeling and marker identification showed that the metabolites in electron transport chain (ETC), redox response, glycolysis, amino acid and nucleotide metabolism were selectively affected by the IPL treatments. Further examinations of the time course, scale, and biochemical functions of these metabolic changes suggested that the degradation of membrane‐bound quinones in the ETC can contribute to many observed changes, including oxidative stress, disruption of intermediary metabolism, nucleotide degradation, and morphological changes. Therefore, the decreases of membrane quinones, especially the depletion of menaquinone‐8, is a prominent and triggering event in IPL‐elicited bactericidal and bacteriostatic effect in E. coli .