The present study evaluated the interactive effects of global change and heavy metals on the growth and development of three soybean [Glycine max (L.) Merrill] cultivars and the consequences on yield and food safety. Soybean cultivars (Alim 3.14 from Argentina, and ES Mentor and Sigalia, from Germany) were grown until maturity in heavy metals polluted soils from the Rhine Valley, Germany, at two CO₂ concentrations (400 and 550 ppm) and heat stress (HS) episodes (9 days with 10 °C higher than maximum regular temperature) during the critical growth period in controlled environmental chambers. Different morpho-physiological parameters, heavy metal concentration in aerial organs, seed quality parameters, and toxicological index were recorded. The results showed that no morphological differences were observed related to CO₂. Moreover, Alim 3.14 showed the highest yield under control conditions, but it was more sensitive to climatic conditions than the German cultivars, especially to heat stress which strongly reduces the biomass of the fruits. Heavy metals concentration in soil exceeds the legislation limits for agricultural soils for Cd and Pb, with 1.6 and 487 mg kg⁻¹ respectively. In all cultivars, soybeans accumulated Cd in its aerial organs, and it could be translocated to fruits. Cd concentration in seeds ranged between 0.6 and 2.4 mg kg⁻¹, which exceed legislation limits and with toxicological risk to potential Chinese consumers. Pb levels were lower than Cd in seeds (0.03–0.17 mg kg⁻¹), and the accumulation were concentrated in the vegetative organs, with 93% of the Pb incorporated. Moreover, pods accumulated 11 times more Pb than seeds, which suggests that they act as a barrier to the passage of Pb to their offspring. These results evidence that soybean can easily translocate Cd, but not Pb, to reproductive organs. No regular patterns were observed in relation to climatic influence on heavy metal uptake.

Human activities lead to increasing concentration of the stable elements cesium (Cs) and strontium (Sr) and their radioactive isotopes in the food chain, where plants play an important part. Here we investigated Plantago major under the influence of long-term exposure to stable Cs and Sr.The plants were cultivated hydroponically in different concentrations of cesium sulfate (between 0.002 and 20 mM) and strontium nitrate (between 0.001 and 100 mM).Uptake of Cs and Sr into leaves was analyzed from extracts by inductively coupled plasma mass spectrometry (ICP-MS). It was increased with increasing external Cs and Sr concentrations. However, the efficiency of Cs and Sr transfer from solution to plants was higher for low external concentrations. Highest transfer factors were 6.78 for Cs and 71.13 for Sr. Accumulation of Sr was accompanied by a slight decrease of potassium (K) and calcium (Ca) in leaves, whereas the presence of Cs in the medium affected only uptake of K.The toxic effects of Cs and Sr were estimated from photosynthetic reactions and plant growth.In leaves, Cs and Sr affected the chlorophyll fluorescence even at their low concentrations. Low and high concentrations of both ions reduced dry weight and length of roots and leaves.The distribution of the elements between the different tissues of leaves and roots was investigated using Energy Dispersive X-Ray microanalysis (EDX) with scanning electron microscope (SEM). Overall, observations suggested differential patterns in accumulating Cs and Sr within the roots and leaves.When present in higher concentrations the amount of Cs and Sr transferred from environment to plants was sufficient to affect some physiological processes. The experimental model showed a potential for P. major to study the influence of radioactive contaminants and their removal from hotspots.

Fine particulate matter (PM₂.₅) is an essential risk factor of chronic obstructive pulmonary disease (COPD). Recent studies showed weak association between PM₂.₅ and COPD incidence, but smokers who exposed to higher PM₂.₅ concentration had more opportunity to gain COPD. Cigarette smoking is the most important risk factor of COPD. Thus, we hypothesized: the role of PM₂.₅ played on cigarette-inflamed airways was more significant than normal airways. The study firstly established an animal model of C57BL/6J mice with cigarette smoke exposure and PM₂.₅ orotracheal administration. After calculating pathological scores, mean linear intercept and mean alveolar area, we found PM₂.₅ aggravated pathological injury of cigarette-inflamed lungs, but the injury on normal lungs was not significant. Meanwhile, inflammatory factors as T-bet, IFN-γ and IL-1α were tested using qRT-PCR and ELISA. The results showed PM₂.₅ aggravated inflammation of cigarette-inflamed lungs, but the effect on normal lungs was not significant. The most important pathogenesis of COPD is abnormal apoptosis in airway epithelium, due to oxidative stress following long-term exposure to cigarette smoke. Then, apoptotic responses were detected in lungs. TUNEL analysis demonstrated that PM₂.₅ promoted DNA fragmentation of cigarette-inflamed lungs, but the effect on normal lungs was not significant. Western-blot and immunohistochemistry showed caspase activated significantly in PM₂.₅-cigarette smoke exposed lungs and activated caspase 3 located mainly on bronchial epithelium. Next, human bronchial epithelial cells were cultured treated with cigarette smoke solution (CSS) with or without PM₂.₅. Z-VAD-FMK, a pan-caspase inhibitor, was used to suppress the activation of caspases. After analyzing cell viability, DNA fragmentation, mitochondrial activities and caspase activities, the results clarified that PM₂.₅ aggravated apoptosis in cigarette-inflamed bronchial epithelial cells and the responses could be suppressed by Z-VAD-FMK. Our results gave a new idea about the mechanism of PM₂.₅ on COPD and inferred cigarette-inflamed airways were more vulnerable to PM₂.₅ than normal airways.

One of the fundamentals in the ecotoxicological studies is the need of data comparison, which can be easily reached with the help of a standardized biological model. In this context, any biological model has been still proposed for the biomonitoring and risk evaluation of freshwaters until now. The aim of this review is to illustrate the ecotoxicological studies carried out with the zebra mussel Dreissena polymorpha in order to suggest this bivalve species as possible reference organism for inland waters. In detail, we showed its application in biomonitoring, as well as for the evaluation of adverse effects induced by several pollutants, using both in vitro and in vivo experiments. We discussed the advantages by the use of D. polymorpha for ecotoxicological studies, but also the possible limitations due to its invasive nature.

Epidemiological studies have demonstrated a strong association of ambient fine particulate matter (PM₂.₅) exposure with the increasing mortality by ischemic heart disease (IHD), but the involved mechanisms remain poorly understood. Herein, we found that the chronic exposure of real ambient PM₂.₅ led to the upregulation of hypoxia-inducible factor-1 alpha (HIF-1α) protein in the myocardium of mice, accompanied by obvious myocardial injury and hypertrophy. Further data from the hypoxia-ischemia cellular model indicated that PM₂.₅-induced HIF-1α accumulation was responsible for the promotion of myocardial hypoxia injury. Moreover, the declined ATP level due to the HIF-1α-mediated energy metabolism remodeling from β-oxidation to glycolysis had a critical role in the PM₂.₅-increased myocardial hypoxia injury. The in-depth analysis delineated that PM₂.₅ exposure decreased the binding of prolyl hydroxylase domain 2 (PHD2) and HIF-1α and subsequent ubiquitin protease levels, thereby leading to the accumulation of HIF-1α. Meanwhile, factor-inhibiting HIF1 (FIH1) expression was down-regulated by PM₂.₅, resulting in the enhanced translocation of HIF-1α to the nucleus. Overall, our study provides valuable insight into the regulatory role of oxygen sensor-mediated HIF-1α stabilization and translocation in PM-exacerbated myocardial hypoxia injury, we suggest this adds significantly to understanding the mechanisms of haze particles-caused burden of cardiovascular disease.