This study aims to evaluate the prenatal developmental toxicity potential of D-allulose produced by genetically engineered Escherichia coli in rats. Given the increasing use of D-allulose in food products, a thorough toxicological assessment is essential to ensure its safety. A prenatal developmental toxicity test in Sprague-Dawley rats was conducted in accordance with the OECD Guidelines Test No. 414 (prenatal developmental toxicity study) and GB 15193.14-2015 (National food safety standards teratogenicity test of the People's Republic of China). Pregnant female rats received repeated doses of 1250, 2500, and 5000 mg/kg bw D-allulose by gavage on Gestation Days (GD) 6-15. A vehicle control (distilled water) and a positive control (cyclophosphamide) were also included. On GD 20, pregnant rats were euthanized, and fetuses were examined for external, soft tissue and skeletal abnormalities. No treatment-related anomalies were observed, indicating that D-allulose did not exhibit prenatal developmental toxic effects. The No-Observed-Adverse-Effect-Level (NOAEL) was determined to be 5000 mg/kg/day.

Nanomaterials have been widely used to scavenge reactive oxygen species (ROS) and relieve mitochondria oxidative damage. However, developing nanomedicines that not only remove ROS but also accelerate the repair of dysfunctional mitochondria remains challenging. This study identifies polyvinylpyrrolidone (PVP)-modified palladium nanoparticles (PdP NPs) as mimics of cytochrome c oxidase (CcO) and superoxide dismutase (SOD), showcasing their potential as multifunctional nanoreactors to activate mitochondria for aging alleviation and neuroprotection. PdP NPs treatment enhances mitochondrial respiratory chain function, scavenges excessive ROS, thus alleviates cellular energy scarcity of aging individuals. Additionally, PdP NPs improve mitochondrial dynamics, promote biogenesis, and induce mitochondrial unfolded protein response (UPRmt), strengthening mitochondrial integrity and homeostasis for better therapeutic outcomes. In vivo evaluations reveal significant anti-aging effects, with the nanozymes notably reducing neurodegeneration and improving neuronal survival. This work highlights PdP NPs as a multifunctional nanotherapeutic platform capable of rewiring mitochondrial metabolism and homeostasis, offering a promising strategy for aging-related disease management.

D-Allulose is a rare monosaccharide structurally similar to D-fructose, characterized by low caloric content and relatively high sweetness. This study aimed to conduct a 90-day oral toxicity test to systemically evaluate the potential toxicological effects of D-allulose produced via a novel one-step fermentation process using genetically engineered Escherichia coli AS10 strain, which was genetically modified to express enzymes involved in the biosynthesis of D-allulose from D-glucose. The objectives were to determine its NOAEL, provide scientific evidence for the safety evaluation of this innovative food ingredient, and meet the regulatory requirements for the safety assessment of a novel process-derived food product. A total of 96 SD rats were randomly divided into four groups (24 rats per group, with equal numbers of males and females): a control group (basal feed) and three treatment groups fed with feed containing 2.5%, 5.0%, and 10.0% D-allulose (corresponding to estimated dietary intakes of 2000, 4000, and 8000 mg/kg body weight per day, respectively, based on an assumed daily feed intake of 8% of body weight) for 90 consecutive days. A comprehensive battery of toxicological assessments was performed on each animal, including measurements on body weight, food consumption, feed efficiency ratios, hematological metrics, serum biochemical profiles, organ weights, and histopathological examinations. No treatment-related mortality or overt toxic symptoms were observed in any group during the study period. Statistically significant differences were noted in partial metrics (e.g., body weight, feed consumption, HCT%, PLT, ALP, TC, and absolute/relative weight of kidney) between treatment groups and control group, but these changes were deemed nontoxicologically significant due to consistency with normal physiological variability (within the historical in-house reference ranges) or lack of corresponding pathological lesions. The NOAEL of D-allulose was established at 8000 mg/kg BW/day in rats, confirming its safety for use as a food ingredient.

Long-term safety, tolerance, and population-specific effects of innovatively fermented D-allulose are lacking in the Chinese population. This study aimed to address these gaps and support its application as a novel food ingredient in China. A 30-day randomized, double-blind, parallel-group design with pre-post comparison trial was conducted, enrolling 50 healthy Chinese adults (high-dose group: 36 g/day, 0.6 g/kg body weight, n = 26; low-dose group: 24 g/day, 0.4 g/kg body weight, n = 24). Gastrointestinal tolerance was monitored via daily questionnaires; systemic safety was evaluated using hematological tests, serum biochemical tests, urinalysis, fecal analysis, and body composition measurements. The incidence of gastrointestinal symptoms was 48.0%, which were mild, transient, and most frequent on Days 1-3, with no significant intergroup differences. All statistically significant changes in safety indicators remained within normal clinical reference ranges. Compared with baseline, the 30-day intervention resulted in reduced red blood cell count, hematocrit, and platelet count, as well as elevated mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration in both groups. For serum biochemical parameters, levels of alkaline phosphatase, gamma-glutamyl transferase, uric acid, total cholesterol, and high-density lipoprotein cholesterol decreased in both groups, while fasting blood glucose was reduced only in high-dose group. Notably, high-dose D-allulose intervention decreased bone mineral density T-scores in participants aged 35 years and older. All statistically significant alterations in the measured indicators remained within normal clinical ranges and were clinically insignificant. This study provides critical safety data to support the planned approval of D-allulose as a novel food ingredient in China in 2025. Its modulation of hematological and serum biochemical parameters suggests effects on hematopoiesis and glycolipid metabolism. Given the limitations of the 30-day intervention duration, relatively modest sample size, and restriction to healthy normal-BMI adults, a provisional safe intake limit of 0.4 g/kg body weight per day is proposed for Chinese adult population, requiring validation in longer-term and larger-scale studies.

L-theanine, a non-protein amino acid naturally occurring in tea leaves, is recognized for its antioxidant, anti-inflammatory, and neuroprotective properties. Despite its known benefits, the mechanisms by which L-theanine influences lifespan extension remain poorly understood. This study investigated the effects of L-theanine on the lifespan of Caenorhabditis elegans and explored the underlying mechanisms. Our findings indicate that L-theanine significantly diminishes the accumulation of advanced glycation end products (AGEs), which are biomarkers closely linked to aging and age-related diseases. Through an AGE-level analysis, we observed that L-theanine, when administered during early adulthood, notably extended the lifespan of Caenorhabditis elegans under both normal and high-glucose-induced stress conditions. L-theanine enhanced the lifespan under typical conditions and provided protective effects against high-glucose-induced stress. A further analysis demonstrated that L-theanine extends the lifespan of Caenorhabditis elegans by modulating the DAF-2/DAF-16 insulin-like signaling pathway and reducing the accumulation of advanced glycation end products (AGEs). In summary, this study identified L-theanine as a potential anti-aging intervention that extends the lifespan by reducing AGE accumulation and regulating insulin-like signaling pathways. These findings provide new insights for developing anti-aging strategies and lay the groundwork for further research on the potential benefits of L-theanine in mammals. Future studies could explore the molecular mechanisms, test L-theanine in mammalian models, and assess the long-term side effects.

Anthraquinones, both naturally occurring and synthetic, are widely distributed in the environment. Recent years, human exposure to 9,10-anthraquinone (9,10-AQ) through contaminated food has been raising significant health concerns due to its potential toxicity upon chronic exposure. Among these, 9,10-AQ has been studied in traditional toxicology, with few of established Points of Departure (PoDs) and Health-Based Guidance Values (HBGV). However, toxicological data for other anthraquinones remain severely limited. Traditional animal experiments are resource-intensive and time-consuming, restricting the feasibility of deriving PoDs and HBGVs for a larger set of compounds and exposures, especially for risk assessment purposes. To address these challenges, New Approach Methodologies (NAMs) were employed and validated by using 9,10-AQ as a reference and representative compound in current study. Hepatocyte hypertrophy via lipid metabolism pathway induced by 9,10-AQ was predicted with applying network toxicology, which was validated using HepG2 cell (0.625-10 μM, for 48 h) combined with high-content imaging showing lipid accumulation induced by 9,10-AQ. The physiologically based toxicokinetic (PBTK) model for rat of 9,10-AQ was developed using in vitro and in silicodata, which was further extrapolated to humans PBTK model, enabling the translation of in vitro concentration–response relationships into in vivo dose–response predictions through PBTK modeling-based reverse dosimetry. From this, a PoD value was derived and converted to a HBGV of 0.0105 mg/kg BW, accounting for uncertainty factors of 100. The NAMs-based HBGV of 9,10-AQ matched well with values derived from animal studies, providing a proof-of-principle of using in vitro-in silicoapproach to predict hepatic lipid metabolic disorder in humans and indicating a good performance of the NAMs. This approach has the potential to be extended to other anthraquinones and derivatives, offering more accurate and reliable human-relevant value (i.e. PoDs, HBGVs), to support Next Generation Risk Assessment (NGRA) of 9,10-AQ and related compounds.

Aging, a universal biological process in complex organisms, is increasingly recognized to be driven by progressive loss of epigenetic information, as proposed in the Information Theory of Aging (ITOA). However, research on anti-aging peptides remains scarce, with most existing efforts confined to derivatives of natural proteins, while systematic design attempts are virtually absent. This limitation not only restricts discovery within the evolutionary sequence space but also hampers the identification of candidates with novel mechanisms and improved efficacy. Here, we present ElixirSeeker2, the first computational framework for de novo design of anti-aging peptides. By integrating modeling of known anti-aging peptides, activity scoring from the IC50 database, and penalty constraints from toxic peptides, ElixirSeeker2 enables large-scale virtual screening and identification of novel peptide candidates. Several lead peptides demonstrated significant effects in delaying cellular senescence, restoring cellular functions in vitro and in enhancing locomotor activity of aged Caenorhabditis elegans . This study not only validates the feasibility of de novo design in anti-aging interventions but also establishes a strategy for the development of next-generation biologics. ### Competing Interest Statement The authors have declared no competing interest. Science and Technology Program of Bei-jing, China, Z231100004523001 Construction Project - Health Toxicology Discipline “Academic Leader”, 02-08 2021 Research Start-up Fund—Fresh Wave, Y030212059003033

The identification of hazardous chemicals is critical for mitigating environmental and health risks, yet existing methods often lack efficiency and accuracy. This study presents HazChemNet, a deep learning model integrating attention-based autoencoders and mixture-of-experts architectures, designed to predict chemical hazardousness from molecular structures. The study utilized a dataset of 2428 hazardous compounds from China’s 2015 hazardous chemical list. Features were derived from molecular fingerprints and physicochemical descriptors, with external validation on 52 unseen chemicals achieving 92.3% accuracy for hazardous and 84.6% for non-hazardous classifications. Experimental validation using C. elegans assays confirmed model predictions for critical compounds. Ablation studies confirmed hydrogen bonding features as pivotal predictors, alongside molecular fingerprints. This work bridges the gap between AI-driven innovation and chemical safety, offering a transformative tool for sustainable industrial practices and proactive risk management in a rapidly evolving global landscape.

Sodium dehydroacetate (DHA-S) is a food additive and preservative. The present study was conducted to investigate the potential toxicity of repeated oral doses of DHA-S. DHA-S was administered orally by gavage to Wistar rats at doses of 0, 50, 100, or 200 mg/kg BW/day for 28 days, after which growth indicators, clinical pathology, organ weights, and histopathology were determined. Body weight and food consumption were significantly reduced at doses of 100 or 200 mg/kg BW, and some hematological indexes and organ weight were significantly affected, particularly in female rats. At a dose of 200 mg/kg BW, the blood coagulation activities were significantly reduced in female rats. At a dose of 100 or 200 mg/kg BW, the main blood biochemical parameters of both sexes were obviously affected. Similar histological changes in the hepatic and renal tissues were observed in both the treated (200 mg/kg BW DHA-S) and control animals. Female rats were more susceptible to most of the toxic effects caused by DHA-S, which further indicating a gender difference in the toxic phenotype profile of rats. Based on these results, the no observed adverse effect level (NOAEL) of DHA-S was determined to be 50 mg/kg BW/day in rats.

Introduction Exposure to fine particulate matter (PM), especially PM 2.5 , can induce various adverse health effects in populations, including diseases and premature death, but the mechanism of its toxicity is largely unknown. Methods Water-soluble components of PM 2.5 (WS-PM 2.5 ) were collected in the north of China in winter, and combined in two groups with the final concentrations of 94 μg/mL (C L group, AQI ≤ 100) and 119 μg/mL (C H group, 100 < AQI ≤ 200), respectively. The acute and long-term toxic effects of WS-PM 2.5 samples were evaluated in several aspects such as development, lifespan, healthspan (locomotion behavior, heat stress tolerance, lipofucin). DAF mutants and genes were applied to verify the action of IIS pathway in WS-PM 2.5 induced-effects. RNA-Sequencing was performed to elucidate the molecular mechanisms, as well as ROS production and Oil red O staining were also served as means of mechanism exploration. Results Body length and lifespan were shortened by exposure to WS-PM 2.5 . Healthspan of nematodes revealed adverse effects evaluated by head thrash, body bend, pharyngeal pump, as well as intestinal lipofuscin accumulation and survival time under heat stress. The abbreviated lifespan of daf-2(e1370) strain and reduced expression level of daf-16 and hsp-16.2 indicated that IIS pathway might be involved in the mechanism. Thirty-five abnormally expressed genes screened out by RNA-Sequencing techniques, were functionally enriched in lipid/lipid metabolism and transport, and may contribute substantially to the regulation of PM 2.5 induced adverse effects in nematodes. Conclusion WS-PM 2.5 exposure induce varying degrees of toxic effects, such as body development, shorten lifespan and healthspan. The IIS pathway and lipid metabolism/transport were disturbed by WS-PM 2.5 during WS-PM 2.5 exposure, suggesting their regulatory role in lifespan determination.

ObjectiveTo provide a reference for food safety risk assessment and safety assurance for the Winter Olympics and Beijing residents， the exposure level and possible health risks of cadmium （Cd） in main foods in the surrounding areas of the 2022 Beijing Winter Olympics were evaluated. MethodsBased on the hazard assessment and limit standard analysis of cadmium， the point assessment method was used to assess the dietary exposure risk of cadmium. The 2019 to 2020 on-site sampling survey data of an urban area of Beijing and Zhangjiakou Chongli area and the 2018 Beijing main food consumption survey data were used in this pre-assessment. ResultsThe cadmium provisional tolerated monthly intake （PTMI） established by joint FAO/WHO Expert Committee on Food Additives （JECFA） was 25 μg/kg·BW. The overall average content of cadmium in various foods was 0.010 6 mg/kg， and the overall rate of exceeding the standard was 0.47%. The average exposure of Beijing residents to cadmium through the main food was 5.92 µg/（kg·BW·m）， accounting for 23.66% of the JECFA-recommended provisional tolerable monthly intake （PTMI） of 25 μg/kg·BW. In addition， cereals and vegetable foods were the main sources of dietary cadmium exposure. According to the current limit of cadmium （LOC） in GB 2762—2017 National Food Safety Standards Limits of contaminants in food， except for these two categories of food， the theoretical exposure to cadmium in the rest of the food did not exceed the PTMI. The estimated LOC for vegetables， grains and cereals is 0.172 and 0.199 mg/kg， both of which were less than the maximum limit value stipulated by the national standard. ConclusionThe main food cadmium exposure of Winter Olympics and Beijing residents is generally at a safe level， and the health risk is relatively low.

目的 采用体内和体外试验,研究常用食品添加剂脱氢乙酸钠(DHA-S)的急性毒性效应.方法 (1)昆明种小鼠单次经口灌胃4640、2150、1000和464 mg/kg·bw剂量的DHA-S,观察中毒症状和死亡情况,确定半数致死量(LD50).(2)秀丽隐杆线虫(野生型N2)L4期幼虫,分别用0～100 mg/ml DHA-S染毒24 h,计数各剂量组线虫死亡率(％).(3)体外培养的中国仓鼠肺细胞(CHL),分别用0～5.0 mg/ml DHA-S染毒24 h,计算各剂量组细胞相对增殖率(％).结果 (1)雌性、雄性小鼠急性经口 LD50分别为1 470和2 000 mg/kg·bw,均属低毒级.(2)线虫的LC50为1.53 mg/ml时,具有毒性.(3)细胞LC50 为1.78 mg/ml,毒性分级为3级,属中等毒性.结论 不同剂量DHA-S急性染毒可对试验动物、模式生物及哺乳动物细胞产生明显的毒性效应.

目的 对副溶血性弧菌的健康危害开展危害评估.方法 本研究基于系统文献检索方法(Systematic Literature Searches,SLS),对副溶血性弧菌的毒理学数据进行系统的文献检索,并根据搜集到的毒理学数据开展健康危害评估.结果 致病性副溶血性弧菌对人体有致病作用.我国现阶段采用食品安全国家标准GB 4789.7-2013《食品微生物学检验副溶血性弧菌检验》和国家标准GB 29921-2013《食品安全国家标准食品中致病菌限量》方法进行检测,判断水产制品副溶血性弧菌标准为:定性实验中为无检出副溶血性弧菌;在定量检测中致病菌可接受水平的限量值为100 MPN/g,最高安全限量值为1000 MPN/g(MPN/g表示每g检样中副溶血性弧菌最可能数).结论 所确定的副溶血性弧菌定性和定量检测标准值,可用于进一步食品安全风险评估.

目的 比较两个厂家生产的总蛋白、白蛋白试剂盒检测大鼠血清是否存在差异.方法 使用两个厂家生产的试剂盒同时检测96个大鼠血清样本的总蛋白和白蛋白含量,并对结果进行统计分析.结果 两个厂家生产的试剂盒检测大鼠血清总蛋白(total protein,TP)、白蛋白(albumin,ALB)差异均有统计学意义(总蛋白t=7.270,P＜0.01;白蛋白t=-10.944,P＜0.01).结论 在开展大鼠血清检测工作中,两个厂家生产的总蛋白、白蛋白试剂均可使用,但对照空白组和研究实验组的血清检测以及实验前后对比时要使用同一厂家生产的试剂盒.

目的 以近交系C57小鼠与远交系KM小鼠为研究对象,应用霍恩氏(Horn)法与上-下法(up-down procedure,UDP)的改良方案,比较硝酸镧(Ⅲ)六水合物的急性经口毒性.方法 参照国内外急性经口毒性试验标准或指南中Horn法与UDP法的设计与计算原理,分别选用90只C57小鼠与KM小鼠(雌雄各半)进行随机分组后,经口灌胃给予预定剂量的硝酸镧(Ⅲ)六水合物水溶液,观察实验动物的中毒表现和死亡情况,计算并比较染毒后1、4、24和48h以及7和14d时的半数致死量(LD50).结果 两种方法观察期结束后,硝酸镧(Ⅲ)六水合物对C57小鼠与KM小鼠的急性经口毒性LD50均在低毒级别(501～5 000 mg/kg·bw),但UDP法的95％可信限范围较广,LD50 计算的准确性没有Horn法高.另外,C57小鼠的中毒表现多在4h内,较KM小鼠(24 h)明显更早,并且动物死亡数量也明显更多,提示C57小鼠的毒性反应更加敏感.并且,同一检测方法下某一小鼠的雄性LD50在各时间点均普遍较低于雌性,存在一定的性别差异.结论 两种方法检测所得硝酸镧(Ⅲ)六水合物对C57小鼠与KM小鼠的急性经口毒性等级均为低毒,且存在明显的性别差异(毒性反应雄性＞雌性),但C57小鼠相对更敏感,提示在进行其他稀土化合物急性毒性检测与评价以及应急毒性检测需缩短观察时间时或可作为优选品系使用.

目的 研究硝酸镧亚急性暴露对C57-ras转基因小鼠神经行为和海马细胞形态学的影响,初步探索ras基因在镧对小鼠海马结构与功能毒性效应中的保护作用.方法 40只C57-ras转基因小鼠随机分为4组(雌雄各半),分别灌胃0、12.5、25和50 mg/kg·bw剂量的硝酸镧六水合物(以镧计算,分别为:4.01、8.02和16.05 mg/kg·bw)28 d;20只同窝野生型小鼠随机分为2组(雌雄各半),分别灌胃0和25 mg/kg·bw剂量的硝酸镧六水合物(以镧计算为8.02 mg/kg·bw)28 d.末次染毒后立即进行爬杆实验、衣架实验、Y迷宫和新物体识别实验,然后采集全血、取脑并分离海马组织.应用电感耦合等离子体质谱仪测定血液和脑中的镧含量,苏木素-伊红(HE)染色法观察海马CA3区病理改变.结果 硝酸镧能被吸收入血并蓄积于小鼠脑组织,海马内的蓄积量高于其他脑区.与同基因型对照小鼠相比,同窝野生型小鼠染镧25 mg/kg·bw组的爬杆时长增加,衣架评分、自发交替反应率和偏好指数均降低(P＜0.05),其海马组织出现病理学改变,CA3区神经元排列层次明显减少且出现紊乱,细胞脱失较为明显,不规则细胞增多;细胞核体积变小,深染,呈核固缩;还可见细胞变性,部分细胞质中尼氏体消失.与同基因型对照组相比,C57-ras转基因小鼠12.5和25 mg/kg·bw染镧组神经行为学表现均未受影响,海马组织未见明显病理改变;50 mg/kg·bw镧组小鼠海马神经元出现与野生型小鼠染镧25 mg/kg·bw组相似的病理损伤.结论 亚急性硝酸镧暴露可以引起小鼠海马CA3区神经元病理改变,并损害小鼠的运动协调和空间学习记忆能力;而ras基因的过表达,在镧所致小鼠海马结构与功能损伤中具有一定的保护作用,其分子机制有待进一步研究.

苯丙(a)蒽(BaA)是一种四环结构的多环芳烃(PAH)类物质,是化石燃料不完全燃烧的副产物,与其他的PAHs以混合物的形式存在.BaA可通过口腔、鼻腔及皮肤等多种途径暴露于人类,对人的主要危害是致癌性.国际癌症研究机构(IARC)根据其分类标准将BaA归为2B类(对人可能致癌).目前尚无充足数据支持通过计算剂量外推斜率因子(slope factor)来完成动物致癌系数与人体致癌系数之间的推导.本文对BaA的致癌性等毒性研究进行系统文献检索与综述,以期为今后进行BaA的健康风险评估提供可靠的毒理学数据基础.

目的 甲基对硫磷(Methyl Parathion,MP)是一种典型的有机磷农药,具有高毒、高效、广谱持久性等特点,在我国于2007年已被禁止使用.本研究以MP的危害识别和危害特征描述为主要内容,开展其健康危害评估,以期为MP的风险评估提供参考.方法 基于系统文献检索获得毒理学及相关数据,对MP进行健康危害评估.结果 MP最小LD50(Wistar大鼠经口)为4 mg/kg·bw,属高毒杀虫剂,被世界卫生组织(WHO)列为Ⅰ a类(剧毒)农药;亚急性/亚慢性试验结果显示MP不仅影响了消化系统(肝)、生殖系统(睾丸)、泌尿系统(肾)、循环系统和神经系统的功能,还造成了器质性病理损伤;基于啮齿类动物和比格犬的试验表明,MP长期毒性表现为体重减轻、震颤、视网膜退化;MP可造成生殖器官器质性和功能性改变,抑制后代的发育潜能;MP作用的主要靶部位是神经系统.此外,MP具有致突变作用,但现有证据尚不能证实MP具有致癌性和致畸性.我国《GB 2763-2021食品中农药最大残留限量》中规定农作物中除仁果类水果(0.01 mg/kg)外,MP最大残留量不得超过0.02 mg/kg,每日允许摄入量(ADI)为0.003 mg/kg·bw.结论 MP暴露对机体造成一定的健康危害,其在粮食、果蔬中的残留及其健康风险仍然是食品安全需要关注的问题之一.

目的 探讨大鼠血清葡萄糖测定分析的影响因素.方法 分别用两台生化分析仪、两种方法的试剂或不同保存条件的大鼠血清样品检测葡萄糖水平.结果 两台生化分析仪测定大鼠血清葡萄糖的结果差异无统计学意义(P>0.05),相关性良好(相关系数r为0.994);两种方法的试剂测定结果差异显著(P<0.01),但相关性良好(相关系数r为0.999);血清即刻测定与4℃冷藏保存4 h、24 h测定的结果差异均无统计学意义(P>0.05),相关性良好(相关系数r为0.999);血清即刻测定与-20℃、-80℃冷冻保存1个月的测定结果差异显著(P<0.01),相关性良好(相关系数r为0.999).结论 进行大鼠血清葡萄糖测定相关动物实验时,应注意所使用的检测仪器设备、试剂方法、样品保存条件的一致性,保证样品检测过程分析阶段的质量.

目的 采用Ames Ⅱ实验评价大气细颗粒物(PM2.5)的遗传毒性以及联合暴露时稀土元素镧对PM2.5遗传毒性的影响.方法 以硝酸镧、供暖期PM2.5样品、非供暖期PM2.5样品、硝酸镧联合供暖期PM2.5样品和硝酸镧联合非供暖期PM2.5样品共5个处理因素分别对测试菌株TA98和TAmix进行染毒,各组均设置16、80、400和2000 μg/ml 4个水平(联合组2种受试物浓度相同);另设置阴性对照组(蒸馏水)和阳性对照组.采用Studento's t检验比较各组阳性孔数与对照组的差异,并分析硝酸镧与两种PM2.5样品之间的联合作用.结果 供暖期和非供暖期样品在相应的剂量条件下,回复突变阳性孔数均明显高于阴性对照组,表现出明显的致突变性;但大鼠肝S9混合物诱导的体外代谢对于二者致突变性的影响明显不同:S9混合物可降低供暖期样品的致突变性,提高非供暖期样品的致突变性.联合暴露时,硝酸镧可影响两种PM2.5样本的致突变性:对于测试菌株TA98,硝酸镧可以降低供暖期和非供暖期样品诱发的自发回变;而对于测试菌株TAmix,硝酸镧可以提高供暖期样品诱发的自发回变,但降低非供暖期样品自发回变.结论 北方某市区PM2.5样本在本实验条件下表现出明显的致突变性;联合暴露时,稀土元素镧可影响PM2.5的致突变作用.