Aquatic ecosystem health is the main concern to increasing pesticides application to control agricultural pests as it is the ultimate receptor of such materials. This study evaluated the impact of new metal-insecticide, the [Mg(hesp)₂(phen)], referred as MgHP, on fish using physiological, genetic, biochemical, and morphological biomarkers. The fish, Prochilodus lineatus, was exposed to 0 (control), 1, 10, 100, 1000 μg L⁻¹ MgHP, for 24 and 96 h. MgHP was not lethal but caused genotoxicity, altered hematological variables and, the activity of antioxidant and biotransformation enzymes and histology of liver, depending on concentration and time exposure. Hematocrit and erythrocyte number (RBC) increased without change hemoglobin content resulting in changes in hematimetric indexes after 24 h; after 96 h, only RBC was changed. Erythrocyte nuclear abnormalities and crenate cells increased after 24 h but, not after 96 h. Erythrocytes and hepatocytes indicated instability in DNA integrity however, the absence of micronuclei suggested DNA damage repairment. After 24 h, the antioxidant defense system and the phase II biotransformation enzyme was responsiveness and catalase activity decreased at high MgHP concentrations; the antioxidant response was triggered after 96 h. Hepatocyte hypertrophy, intracellular cytoplasmic substances, cytoplasm degeneration, melanomacrophage and hyperemia increased in fish exposed from 10 μg L⁻¹ to higher MgHP concentrations; the organ alteration index increased as MgHP concentration increased showing dose-dependence. Most of hematological and genotoxic effects occurred after 24 h exposure evidencing potential recover capability of organism by activation of the antioxidant defense system and DNA repairment mechanisms. Nevertheless, the histopathological changes in the liver was maintained over time at high MgHP concentrations, a concentration usually no environmental relevant. In conclusion, this data reinforced the importance of continuing research on MgHP effects in other organisms considering the promising use of such compound to control the leaf-cutter ants and other insects.

Perfluorooctane sulfonate (PFOS) has been widely used as a surface coating for household products. It still exists in living environments despite being restricted, due to its bioaccumulation and long half-life. Studies have shown that PFOS has the ability to induce adipogenic differentiation of human cells. Human mesenchymal stem cells (hMSCs) distributed within the adipose tissue might be a potential target of accumulated PFOS. However, traditional end-point toxicity assays failed to examine the subtle changes of cellular function exposed to low-dose persistent organic pollutants in real time. In the present work, highly sensitive and long-retained (more than 30 days) fluorescence based polymeric nanosensors were developed and employed for real-time assessment of cellular functions. hMSCs were engineered with sensor molecules encapsulated poly (lactic-co-glycolic acid) (PLGA) particles. Once internalized by hMSCs, PLGA particles continuously release and replenish sensor molecules to cytoplasm, resulting in prolonged fluorescence signal against photo bleaching and dilution by exocytosis. With this method, the dynamic changes of viability, ROS induction, and adipogenic differentiation related mRNA expression of hMSCs were monitored. PFOS with the concentration as low as 0.1 μM can induce cellular ROS and enhance the PPARγ and ap2 mRNA expression, suggesting the effect on promoting adipogenic differentiation of hMSCs.

Fungi have an exceptional capability to flourish in presence of heavy metals and pesticide. However, the mechanism of bioremediation of pesticide (lindane) and multimetal [mixture of cadmium (Cd), chromium (Cr), copper (Cu), nickel (Ni), lead (Pb), zinc (Zn)] by a fungus is little understood. In the present study, Aspergillus fumigatus, a filamentous fungus was found to accumulate heavy metals in the order [Zn(98%)>Pb(95%)>Cd(63%)>Cr(62%)>Ni(46%)>Cu(37%)] from a cocktail of 30 mg L⁻¹ multimetal and lindane (30 mg L⁻¹) in a composite media amended with 1% glucose. Particularly, Pb and Zn uptake was enhanced in presence of lindane. Remarkably, lindane was degraded to 1.92 ± 0.01 mg L⁻¹ in 72 h which is below the permissible limit value (2.0 mg L⁻¹) for the discharge of lindane into the aquatic bodies as prescribed by European Community legislation. The utilization of lindane as a cometabolite from the complex environment was evident by the phenomenal growth of the fungal pellet biomass (5.89 ± 0.03 g L⁻¹) at 72 h with cube root growth constant of fungus (0.0211 g¹/³ L⁻¹/³ h⁻¹) compared to the biomasses obtained in case of the biotic control as well as in presence of multimetal complex without lindane. The different analytical techniques revealed the various stress coping strategies adopted by A. fumigatus for multimetal uptake in the simultaneous presence of multimetal and pesticide. From the Transmission electron microscope coupled energy dispersive X-ray analysis (TEM-EDAX) results, uptake of the metals Cd, Cu and Pb in the cytoplasmic membrane and the accumulation of the metals Cr, Ni and Zn in the cytoplasm of the fungus were deduced. Fourier-transform infrared spectroscopy (FTIR) revealed involvement of carboxyl/amide group of fungal cell wall in metal chelation. Thus A. fumigatus exhibited biosorption and bioaccumulation as the mechanisms involved in detoxification of multimetals.

Epidemiological studies and animal experiments have suggested that exposure to Di-(2-ethylhexyl) phthalate (DEHP) is strongly associated with an increase in blood pressure. However, the mechanisms that result in the detrimental effects of DEHP exposure on blood pressure are unclear. In our study, mice were orally exposed to DEHP dosages of 0.1, 1, 10 mg/kg/day for 6 weeks. The results showed that DEHP could induce a significant increase in systolic blood pressure (SBP) and heart rate, and a significant thickening of the ventricular wall. To explore the underlying mechanism, we measured the level of: angiotensin converting enzyme (ACE); bradykinin B2 receptor (BK2R); endothelial nitric oxide synthase (eNOS); bradykinin and Ca²⁺ in cardiac cytoplasm as well as in serum nitric oxide (NO). The results suggested that DEHP could induce an increase in ACE levels, and a decrease in bradykinin levels. Moreover, BK2R, Ca²⁺, eNOS and NO decreased when mice were exposed to 10 mg/kg/day DEHP. Interestingly, 5 mg/kg/day angiotensin converting enzyme inhibitor (ACEI) treatment inhibited the increase in blood pressure, and inhibited the decrease in the levels of BK2R, Ca²⁺, eNOS, and NO, that were induced by DEHP exposure. Our results suggest that DEHP might increase blood pressure by activating ACE expression, and inhibiting the bradykinin-NO pathway.

The ubiquity of pollutants, such as agrochemicals and heavy metals, constitute a serious risk to human health. To evaluate the induction of DNA damage and programmed cell death (PCD), root cells of Allium cepa and Vicia faba were treated with two organophosphate insecticides (OI), fenthion and malathion, and with two heavy metal (HM) salts, nickel nitrate and potassium dichromate. An alkaline variant of the comet assay was performed to identify DNA breaks; the results showed comets in a dose-dependent manner, while higher concentrations induced clouds following exposure to OIs and HMs. Similarly, treatments with higher concentrations of OIs and HMs were analyzed by immunocytochemistry, and several structural characteristics of PCD were observed, including chromatin condensation, cytoplasmic vacuolization, nuclear shrinkage, condensation of the protoplast away from the cell wall, and nuclei fragmentation with apoptotic-like corpse formation. Abiotic stress also caused other features associated with PCD, such as an increase of active caspase-3-like protein, changes in the location of cytochrome C (Cyt C) toward the cytoplasm, and decreases in extracellular signal-regulated protein kinase (ERK) expression. Genotoxicity results setting out an oxidative via of DNA damage and evidence the role of the high affinity of HM and OI by DNA molecule as underlying cause of genotoxic effect. The PCD features observed in root cells of A. cepa and V. faba suggest that PCD takes place through a process that involves ERK inactivation, culminating in Cyt C release and caspase-3-like activation. The sensitivity of both plant models to abiotic stress was clearly demonstrated, validating their role as good biosensors of DNA breakage and PCD induced by environmental stressors.

The environmental safety of cerium (Ce) applications in many fields has been debated for almost a century because the cellular effects of environmental Ce on living organisms remain largely unclear. Here, using new, interdisciplinary methods, we surprisingly found that after Ce(III) treatment, Ce(III) was first recognized and anchored on the plasma membrane in leaf cells. Moreover, some trivalent Ce(III) was oxidized to tetravalent Ce(IV) in this organelle, which activated pinocytosis. Subsequently, more anchoring sites and stronger valence-variable behavior on the plasma membrane caused stronger pinocytosis to transport Ce(III and IV) into the leaf cells. Interestingly, a great deal of Ce was bound on the pinocytotic vesicle membrane; only a small amount of Ce was enclosed in the pinocytotic vesicles. Some pinocytic vesicles in the cytoplasm were deformed and broken. Upon breaking, pinocytic vesicles released Ce into the cytoplasm, and then these Ce particles self-assembled into nanospheres. The aforementioned special behaviors of Ce decreased the fluidity of the plasma membrane, inhibited the cellular growth of leaves, and finally, decreased plant yield. In summary, our findings directly show the special cellular behavior of Ce in plant cells, which may be the cellular basis of plant yield reduction induced by environmental Ce.

In bacteria a metal may be defined as bioavailable if it crosses the cytoplasmic membrane to reach the cytoplasm. Once inside the cell, specific metal resistance systems may be triggered. In this research, specific metal resistance genes were used to estimate metal bioavailability in sediment microbial communities. Gene levels were measured by quantitative PCR and correlated to metals in sediments using five different protocols to estimate dissolved, particle-adsorbed and occluded metals. The best correlations were obtained with czcA (a Cd/Zn/Co efflux pump) and Cd/Zn adsorbed or occluded in particles. Only adsorbed Co was correlated to czcA levels. We concluded that the measurement of czcA gene levels by quantitative PCR is a promising tool which may complement the classical approaches used to estimate Cd/Zn/Co bioavailability in sediment compartments.

Antibiotic resistance in environmental matrices becomes urgently significant for public health and has been considered as an emerging environmental contaminant. In this work, the ampicillin-resistant Escherichia coli (AR E. coli) and corresponding resistance genes (blaTEM₋₁) were effectively eliminated by the electrocatalytic process, and the dissemination risk of antibiotic resistance was also investigated. All the AR E. coli (∼8 log) was inactivated and 8.17 log blaTEM₋₁ was degraded by the carbon nanotubes/agarose/titanium (CNTs/AG/Ti) electrode within 30 min. AR E. coli was inactivated mainly attributing to the damage of cell membrane, which was attacked by reactive oxygen species and subsequent leakage of intracellular cytoplasm. The blaTEM₋₁ was degraded owing to the strand breaking in the process of electrocatalytic degradation. Furthermore, the dissemination risk of antibiotic resistance was effectively controlled after being electrocatalytic treatment. This study provided an effective electrocatalytic technology for the inactivation of antibiotic resistant bacteria and control of antibiotic resistance dissemination risk in the aqueous environment.

The broad application of triclosan (TCS) and triclocarban (TCC) as antimicrobials in household and personal care products has led to the concerns regarding their human health risk and environmental impact. Although many studies have examined the toxicological effects of these compounds to a wide range of aquatic organisms from algae to fish, their potential toxicity to an important model organism the nematode Caenorhabditis elegans has never been systematically investigated. Here we assessed the toxicological effects of TCS and TCC in C. elegans using endpoints from organismal to molecular levels, including lethality, reproduction, lifespan, hatching, germline toxicity, and oxidative stress. L4 stage or young adult worms were exposed to TCS or TCC and examined using above-mentioned endpoints. Both TCS and TCC showed acute toxicity to C. elegans, with 24-h LC50s of 3.65 (95% CI: 3.15, 4.3) mg/L and 0.91 (95% CI: 0.47, 1.53) mg/L, respectively. TCS at 0.1–2 mg/L and TCC at 0.01–0.5 mg/L, respectively, induced concentration dependent reduction in the worm's reproduction, lifespan, and delay in hatching. Using a DAF-16:GFP transgenic strain, we found both compounds induced oxidative stress in the worm, indicated by the relocalization of DAF-16:GFP from cytoplasm to the nucleus upon exposure. Germline toxicity of the two compounds was also demonstrated using a xol-1:GFP transgenic strain. These findings suggest that TCS and TCC induce systemic toxic effects in C. elegans. Further studies are needed to elucidate the potential mechanisms of toxicity of these antimicrobials in the model organism, especially their potential endocrine disruption effects.

Microplastics (MPs) have become a global concern as a key environmental pollutant. MPs are widely found in oceans, rivers, bottled water, plastic-packaged foods, and toiletries. The ocular surface is the exposed mucosal tissue, which comes in contact with MP particles contained in toiletries, tap water, cosmetics, and air. However, the effects of MPs on ocular surface health are still unclear. In this study, the toxic effects of polystyrene MPs (PS-MPs) on the ocular surface in vivo and in vitro were explored. The results demonstrated that 50 nm or 2 μm PS-MPs, following exposure for 48 h appeared in the cytoplasm of two kinds of eye cells in vitro and caused a concentration dependent reduction in cell viability, further causing oxidative stress and cell apoptosis. In addition, after treatment for 2 or 4 weeks, 50 nm and 2 μm PS-MPs were deposited in the conjunctival sac of mice. After 2 and 4 weeks of PS-MP treatment, the number of goblet cells in the lower eyelid conjunctival sac decreased to 65% and 40% of that in the control group, respectively. Moreover, dry eye like ocular surface damage and inflammation of conjunctiva and lacrimal gland in mice were observed. In conclusion, this study revealed that PS-MPs could cause ocular surface dysfunctions in mice, thus providing a new perspective for the toxic effects of MPs on ocular surface.