2,4,6-trinitrotoluene causes mitochondrial toxicity in Caenorhabditis elegans by affecting electron transport.

As a typical energetic compound widely used in military activities, 2,4,6-trinitrotoluene (TNT) has attracted great attention in recent years due to its heavy pollution and wide distribution in and around the training facilities, firing ranges, and demolition sites. However, the subcellular targets and the underlying toxic mechanism of TNT remain largely unknown. In this study, we explored the toxic effects of TNT biological reduction on the mitochondrial function and homeostasis in Caenorhabditis elegans (C. elegans). With short-term exposure of L4 larvae, 10-1000 ng/mL TNT reduced mitochondrial membrane potential and adenosine triphosphate (ATP) content, which was associated with decreased expression of specific mitochondrial complex involving gas-1 and mev-1 genes. Using fluorescence-labeled transgenic nematodes, we found that fluorescence expression of sod-3 (muls84) and gst-4 (dvls19) was increased, suggesting that TNT disrupted the mitochondrial antioxidant defense system. Furthermore, 10 ng/mL TNT exposure increased the expression of the autophagy-related gene pink-1 and activated mitochondrial unfolded protein response (mt UPR), which was indicated by the increased expression of mitochondrial stress activated transcription factor atfs-1, ubiquitin-like protein ubl-5, and homeobox protein dve-1. Our findings demonstrated that TNT biological reduction caused mitochondrial dysfunction and the development of mt UPR protective stress responses, and provided a basis for determining the potential risks of energetic compounds to living organisms.

Multi-generation reproductive toxicity of RDX and the involved signal pathways in Caenorhabditis elegans.

As one of the most frequently used explosives, hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX) can cause persistent pollution in the environment, leading to the potential ecological threat crossing the generations. In this study, we employed Caenorhabditis elegans to explore the toxic effects of RDX on the parental and offspring worms and the involved signaling pathways. Exposure up to 1000 ng/mL of RDX produced a significant increase in reactive oxygen species (ROS) production, germ cell apoptosis, and decrease in eggs laid. Various mutants were used to demonstrate the RDX-induced apoptosis signaling pathway, and the metabolism of RDX in the nematodes was found related to cytochrome P450 and GST through RNA sequencing. Exposure of parental worms to RDX produced significant reproductive toxicity in F1 and F2, but was recovered in F3 and F4. The transgenerational effects were associated with the decreased expression of met-2, spr-5, and set-2. Our findings revealed the signaling pathways related to the reproductive toxicity caused by RDX in C. elegans and their future generations, which provided the basis for further exploration of the ecological risks of energetic compounds in the environment.

Multi-locus deletion mutation induced by silver nanoparticles: Role of lysosomal-autophagy dysfunction.

Due to the rapid production growth and a wide range of applications, safety concerns are being raised about the genotoxic properties of silver nanoparticles (AgNPs). In this research, we found AgNPs induced a size-dependent genotoxicity via lysosomal-autophagy dysfunction in human-hamster hybrid (AL) cells. Compared with 25 nm and 75 nm particles, 5 nm AgNPs could accentuate the genotoxic responses, including DNA double-strand breaks (DSBs) and multi-locus deletion mutation, which could be significantly enhanced by autophagy inhibitors 3-methyl adenine (3-MA), Bafilomycin A1 (BFA), and cathepsin inhibitors, respectively. The autophagy dysfunction was closely related to the accumulation of 5 nm AgNPs in the lysosomes and the interruption of lysosome-autophagosome fusion. With lysosomal protective agent 3-O-Methylsphingomyelin (3-O-M) and endocytosis inhibitor wortmannin, the reactivation of lysosomal function and the recovery of autophagy significantly attenuated AgNP-induced genotoxicity. Our data provide clear evidence to illustrate the role of subcellular targets in the genotoxicity of AgNPs in mammalian cells, which laid the basis for better understanding the health risk of AgNPs and their related products.

Connection between health risk and heavy metals in agricultural soils of China: a study based on current field investigations.

Heavy metal pollution in agricultural soil is a threat to people's health and sustainable development. However, there is currently no nationwide health risk assessment in China. In this study, we performed a preliminary assessment of heavy metals in agricultural soils of the Chinese mainland, and found obvious carcinogenic risks (total lifetime carcinogenic risk (TLCR) > 1 × 10-5). A similar spatial distribution pattern was found in soil heavy metal and the mortality of esophagus and stomach cancers. Combining the potential carcinogenic risk assessed by LCR for individual heavy metal with Pearson correlation, Geographical Detector (q statistic > 0.75 for TLCR, p < 0.05), and redundancy analysis (RDA), it was found that long-term exposure and intake route of heavy metals exceeding the maximum safety threshold (Health Canada standard) may induce digestive system (esophagus, stomach, liver, and colorectum) cancers in rural populations. Through Partial Least Squares Path Model (PLS-PM), it was also revealed that the LCR of heavy metals was closely related to the soil environmental background (path coefficients = 0.82), which in turn was affected by factors such as economic development and pollution discharge. The current research results highlight the potential carcinogenic risk to the digestive system associated with low-dose and long-term exposure to heavy metals in agricultural soils, and policymakers should propose countermeasures and solutions according to the local conditions.

Transgenerational effects of diesel particulate matter on Caenorhabditis elegans through maternal and multigenerational exposure.

Diesel particulate matter (DPM) is a dominant contaminant in fine particulate matters (PM2.5) and has been proved to induce serious harmful effects to human beings, including lung cancer, allergic, and chronic bronchitis. However, little attention has been paid to understand the transgenerational effects of DPM. In the present study, we focused on the transgenerational effects of DPM in the model organism Caenorhabditis elegans (C. elegans) exposed in either maternal generation (F0) or consecutive generations (F0-F5). In maternal exposure manner, 0.1 and 1.0 µg/mL DPM significantly increased the germ cell apoptosis at F0 generation, while the number of apoptotic germ cells at F1-F5 generation were gradually recovered back to control level. The brood size were significantly reduced by DPM at F2 generation and recovered to control level at F3-F5 generations. In continuous exposure manner, although 0.1 and 1.0 µg/mL DPM induced significant germ cell apoptosis in F0 generation, there was no difference between F0 and other generations. Continuous exposure to DPM at 0.1 and 1.0 µg/mL impaired the brood size in F2 to F5 generations. Using a series of loss-of-function mutant strains, we found that cep-1 (w40), hus-1 (op241), and mitogen-activated protein kinase (MAPK) related signaling pathway genes were involved in DPM-induced apoptosis. Our results clearly demonstrated that the adverse effects of DPM could be passed on through long-term multigenerational exposure and DNA damage checkpoint genes and MAPK signal pathway played an essential role in response to DPM induced development and reproduction toxicity.

Aging-independent and size-dependent genotoxic response induced by titanium dioxide nanoparticles in mammalian cells.

Titanium dioxide nanoparticles (TiO2 NPs) are subjected to various transformation processes (chemical, physical and biological processes) in the environment, potentially affecting their bioavailability and toxic properties. However, the size variation of TiO2 NPs during aging process and subsequent effects in mammalian cells are largely unknown. The aim of this study was to illustrate the adverse effects of TiO2 NPs in different sizes (5, 15 and <100 nm) during aging process on human-hamster hybrid (AL) cells. There was an aging-time dependent enhancement of average hydrodynamic size in TiO2 NPs stock suspensions. The cytotoxicity of fresh TiO2 NPs increased in a size-dependent manner; in contrast, their genotoxicity decreased with the increasing sizes of NPs. No significant toxicity difference was observed in cells exposed to either fresh or 60 day-aged TiO2 NPs. Both Fresh and aged TiO2 NPs efficiently induced mitochondrial dysfunction and activated Caspase-3/7 in a size-dependent manner. Using mitochondrial-DNA deficient (ρ0) AL cells, we further discovered that mitochondrial dysfunction made significant contribution to the size-dependent toxicity induced by TiO2 NPs during the aging process. Taken together, our data indicated that TiO2 NPs could significantly induced the cytotoxicity and genotoxicity in an aging time-independent and size-dependent manner, which were triggered by mitochondrial dysfunction. Our study suggested the necessity to include size as an additional parameter for the cautious monitoring of TiO2 NPs disposal before entering the environment.

Mechanisms involved in the impact of engineered nanomaterials on the joint toxicity with environmental pollutants.

Emerging nanoscience and nanotechnology inevitably facilitate discharge of engineered nanomaterials (ENMs) into the environment. Owing to their versatile physicochemical properties, ENMs invariably come across and interact with various pollutants already existing in the environment, leading to considerable uncertainty regarding the risk assessment of pollutants. Nevertheless, the underlying mechanisms of the complicated joint toxicity are still largely unexplored. This review aims to aid in understanding the interaction of ENMs and pollutants from the perspective of ecological and environmental health risk assessment. Based on related research published from 2005 to 2018, this review focuses on summarizing the effect of ENMs on the toxicity of pollutants both in vivo and in vitro. Physicochemical interaction appears as a main factor affecting ENMs-pollutants joint toxicity, with the mechanisms and the resultants for ENM-pollutant adsorption been illustrated. Cellular and molecular mechanisms involved in the joint toxicity of ENMs and pollutants are discussed, including the effect of ENMs on the bioaccumulation, biodistribution, and metabolism of pollutants, as well as the defense responses of organisms against such pollutants. Future in-depth investigation are suggested to focus on further exploring biological mechanisms (especially for the antagonized effect of ENMs against pollutants), using more advanced mammalian models, and paying more attention to the realistic exposure scenarios.

TiO2 nanoparticles enhance bioaccumulation and toxicity of heavy metals in Caenorhabditis elegans via modification of local concentrations during the sedimentation process.

Unintentionally released titanium dioxide nanoparticles (TiO2 NPs) may co-occur with pre-existing heavy metal pollutants in aquatic environments. However, the interactions between NPs and heavy metals (HMs) and their co-effects in living organisms are largely unknown. The aim of this investigation was to illustrate the influence of TiO2 NPs (5 and 15 nm) on the bioaccumulation and toxicity of cadmium (Cd), arsenate (As(III)), and nickel (Ni) in Caenorhabditis elegans (C. elegans) during the process of sedimentation in aquatic environment. Our data showed that HMs accelerated the aggregation of TiO2 NPs. The rapid aggregation and sedimentation of TiO2 NPs changed the vertical distribution of HMs through adsorption and induced increased and prolonged exposure of benthic species. Aggregate particle size along with ionic strength were the major factors affecting the rate of sedimentation. TiO2 NPs at non-toxic concentrations efficiently enhanced the bioaccumulation and reproductive toxicity of HMs to C. elegans in a dose- and size-dependent manner; however, the effect of TiO2 NPs on As(III) was obviously lower than that on two valence metals. These data provided clear evidence that TiO2 NPs could serve as environmental regulators to significantly facilitate the toxicity and the accumulation of HMs in C. elegans, indicating that the interaction and fate of TiO2 NPs and HMs on their co-toxic responses during the sedimentation should be considered as a necessary and integral part of risk assessment in the ecological system.

Graphene Oxide Attenuates the Cytotoxicity and Mutagenicity of PCB 52 via Activation of Genuine Autophagy.

Graphene oxide (GO), owing to its large surface area and abundance of oxygen-containing functional groups, is emerging as a potential adsorbent for polychlorinated biphenyls (PCBs), which accumulate over time and are harmful to both natural ecosystems and human health. However, the effect of GO against PCB-induced toxicity remains largely unexplored. The present study aimed to investigate the protective effect of GO against PCB 52 induced cytotoxic and genotoxic response in mammalian cells at various exposure conditions and clarify the protective role of autophagy. Pretreatment with GO dramatically decreased PCB 52 induced cytotoxicity and CD59 gene mutation in human-hamster hybrid (AL) cells. The toxic response in cells either pretreated with PCB 52 and then treated with GO or concurrently treated with GO and PCB 52 did not differ significantly from the toxic response in the cells treated with PCB 52 alone. Using autophagy inhibitors (3-methyladenine and wortmannin) and inducers (trehalose and rapamycin), we found that genuine autophagy induced by GO was involved in decreasing PCB 52 induced toxicity. These findings suggested that GO has an antagonistic effect against the toxicity of PCB 52 mainly by triggering a genuine autophagic process, which might provide new insights into the potential application of GO in PCB disposal and environmental and health risk assessment.

Trace elements (Cu, Zn, and Hg) and δ13C/δ15N in seabird subfossils from three islands of the South China Sea and its implications.

Seabird subfossils were collected on three islands of the Xisha Archipelago, South China Sea. Via elemental analysis, we identified that bird guano was a significant source for heavy metals Cu, Zn, and Hg. Cu and Zn levels in these guano samples are comparable to their levels in wildbird feces, but guano Hg was lower than previously reported. Trophic positions significantly impacted transfer efficiency of heavy metals by seabirds. Despite of a common source, trace elements, as well as stable isotopes (i.e., guano δ(13)C and collagen δ(15)N), showed island-specific characteristics. Bird subfossils on larger island had relatively greater metal concentrations and revealed higher trophic positions. Partition of element and isotope levels among the islands suggested that transfer efficacy of seabirds on different islands was different, and bird species were probably unevenly distributed among the islets. Island area is possibly a driving factor for distributions of seabird species.

Endosulfan isomers and sulfate metabolite induced reproductive toxicity in Caenorhabditis elegans involves genotoxic response genes.

Endosulfan is enlisted as one of the persistent organic pollutants (POPs) and exists in the form of its α and ß isomers in the environment as well as in the form of endosulfan sulfate, a toxic metabolite. General endosulfan toxicity has been investigated in various organisms, but the effect of the isomers and sulfate metabolites on reproductive function is unclear. This study was aimed at studying the reproductive dysfunction induced by endosulfan isomers and its sulfate metabolite in Caenorhabditis elegans (C. elegans). We also determined a role for the DNA-damage-checkpoint gene hus-1. Compared to ß-endosulfan and its sulfate metabolite, α-endosulfan caused a dramatically higher level of germ cell apoptosis, which was regulated by DNA damage signal pathway. Both endosulfan isomers and the sulfate metabolite induced germ cell cycle arrest. Loss-of-function studies using hus-1, egl-1, and cep-1 mutants revealed that hus-1 specifically influenced the fecundity, hatchability, and sexual ratio after endosulfan exposure. Our data provide clear evidence that the DNA-checkpoint gene hus-1 has an essential role in endosulfan-induced reproductive dysfunction and that α-endosulfan exhibited the highest reproductive toxicity among the different forms of endosulfan.

Parental treatment with selenium protects Caenorhabditis elegans and their offspring against the reproductive toxicity of mercury.

Mercury (Hg) is one of the major pollutants in the environment, which requires effective countermeasures to manage its risk to both human health and the ecosystem. The antagonistic effect of selenium (Se) against methyl mercury (MeHg) and HgCl2 was evaluated using parent and offspring Caenorhabditis elegans (C. elegans) in this study. Through designated acute exposure of 24 h, our results showed that both MeHg and HgCl2 induced dose-dependent reproductive toxicity, including increased germ cell apoptosis, decrease in the number of oocytes, brood size, and sperm activation. The increased germ cell apoptosis was even higher in F1 and F2 generations, but returned to control level in F3 generation. Pretreatment with Se significantly suppressed the reproductive toxicity caused by Hg in both parental worms and their offspring, but had little influence on Hg accumulation. The protective role of Se was found closely related to the chemical forms of Hg: mtl-1 and mtl-2 genes participated in reducing the toxicity of HgCl2, while the gst-4 gene was involved in the reduced toxicity of MeHg. The formation of Se-Hg complex and the antioxidant function of Se were considered as possible antagonistic mechanisms. Our data indicated that pretreatment with Se could effectively protect C. elegans and their offspring against the reproductive toxicity of Hg in different chemical forms, which provided a reference for the prevention of Hg poisoning and essential information for better understanding the detoxification potential of Se on heavy metals.

Arsenic species in soil profiles from chemical weapons (CWs) burial sites of China: Contamination characteristics, degradation process and migration mechanism.

In this study, soil profiles and pore water from Japanese abandoned arsenic-containing chemical weapons (CWs) burial sites in Dunhua, China were analyzed to understand the distribution of arsenic (As) contamination, degradation, and migration processes. Results of As species analysis showed that the As-containing agents underwent degradation with an average rate of 87.55 ± 0.13%, producing inorganic pentavalent arsenic (As5+) and organic arsenic such as 2-chlorovinylarsonic acid (CVAOA), triphenylarsenic (TPA), and phenylarsine oxide (PAO). Organic arsenic pollutants accounted for 1.27-18.20% of soil As. In the vertical profiles, total As concentrations peaked at about 40-60 cm burial depth, and the surface agricultural soil exhibited moderate to heavy contamination level, whereas the contamination level was insignificant below 1 m, reflecting As migration was relatively limited throughout the soil profile. Sequential extraction showed Fe/Al-bound As was the predominant fraction, and poorly-crystalline Fe minerals adsorbed 33.23-73.13% of soil As. Oxygen-susceptible surface soil formed poorly-crystalline Fe3+ minerals, greatly reducing downward migration of arsenic. However, the reduction of oxidizing conditions below 2 m soil depth may promote As activity and require attention.

Zinc oxide/graphene oxide nanocomposites specifically remediated Cd-contaminated soil via reduction of bioavailability and ecotoxicity of Cd.

From both environment and health perspectives, sustainable management of ever-growing soil contamination by heavy metal is posing a serious global concern. The potential ecotoxicity of cadmium (Cd) to soil and ecosystem seriously threatens human health. Developing efficient, specific, and long-term remediation technology for Cd-contaminated soil is impending to synchronously minimize the bioavailability and ecotoxicity of Cd. In the present study, zinc oxide/graphene oxide nanocomposite (ZnO/GO) was developed as a novel amendment for remediating Cd-contaminated soil. Our results showed that ZnO/GO effectively decreased the available soil Cd content, and increased pH and cation exchange capacity (CEC) in both Cd-spiked standard soil and Cd-contaminated mine field soil through the interaction between ZnO/GO and soil organic acids. Using Caenorhabditis elegans (C. elegans) as a model organism for soil safety evaluation, ZnO/GO was further proved to decrease the ecotoxicity of Cd-contaminated soil. Specifically, ZnO/GO promoted Cd excretion and declined Cd storage in C. elegans by increasing the expression of gene ttm-1 and decreasing the level of gene cdf-2, which were responsible for Cd transportation and Cd accumulation, respectively. Moreover, the efficacy of ZnO/GO in remediating the properties and ecotoxicity of Cd-contaminated soil increased gradually with the time gradient, and could maintain a long-term effect after reaching the optimal remediation efficiency. Our findings established a specific and long-term strategy to simultaneously improve soil properties and reduce ecotoxicity of Cd-contaminated soil, which might provide new insights into the potential application of ZnO/GO in soil remediation for both ecosystem and human health.

Spatial-vertical variations of energetic compounds and microbial community response in soils from an ammunition demolition site in China.

Ammunition-related activities have caused severe energetic compound (EC) contamination and pose serious risks to ecosystems. However, little is known regarding the spatial-vertical variations of ECs or their migration in soils at ammunition demolition sites. Although the toxic effect of some ECs to microorganisms have been reported through laboratory simulations, the responses of indigenous microbial communities to ammunition demolition activities are unclear. In this study, the spatial-vertical variations of ECs in 117 topsoil samples and three soil profiles from a typical ammunition demolition site in China were studied. Heavy contamination of ECs was concentrated in the top soils of the work platforms, and ECs were also detected in the surrounding area and nearby farmland. ECs showed different migration characteristics in the 0-100 cm soil layer of the different soil profiles. Demolition activities and surface runoff play critical roles in the spatial-vertical variations and migration of ECs. These findings suggest that ECs are able to migrate from the topsoil to the subsoil and from the core demolition area to further ecosystems. The work platforms exhibited lower microbial diversity and different microbiota compositions compared to the surrounding areas and farmlands. Using the random forest analysis, pH and 1,3,5-trinitrobenzene (TNB) were characterized as the most important factors affecting microbial diversity. Network analysis revealed that Desulfosporosinus was highly sensitive to ECs and may be a unique indicator of EC contamination. These findings provide key information in understanding EC migration characteristics in soils and the potential threats to indigenous soil microorganisms in ammunition demolition sites.

Molecular transformation of organic nitrogen in Antarctic penguin guano-affected soil.

Organic nitrogen (ON) is an important participant in the Earth's N cycle. Previous studies have shown that penguin feces add an abundance of nutrients including N to the soil, significantly changing the eco-environment in ice-free areas in Antarctica. To explore the molecular transformation of ON in penguin guano-affected soil, we collected guano-free weathered soil, modern guano-affected soil from penguin colonies, ancient guano-affected soil from abandoned penguin colonies, and penguin feces from the Ross Sea region, Antarctica, and Fourier transform ion cyclotron mass spectrometry (FT-ICR MS) was used to investigate the chemical composition of water-extractable ON. By comparing the molecular compositions of ON among different samples, we found that the number of ON compounds (>4,000) in weathered soil is minimal, while carboxylic-rich alicyclic-like molecules (CRAM-like) are dominant. Penguin feces adds ON into the soil with > 10,000 CHON, CHONS and CHN compounds, including CRAM-like, lipid-like, aliphatic/ peptide-like molecules and amines in the guano-affected soil. After the input of penguin feces, macromolecules continue to degrade, and other ON compounds tend to be oxidized into relatively stable CRAM-like molecules, this is an important transformation process of ON in guano-affected soils. We conclude the roles of various forms of ON in the N cycle are complex and diverse. Combined with previous studies, ON eventually turns into inorganic N and is lost from the soil. The lost N ultimately returns to the ocean and the food web, thus completing the N cycle. Our study preliminarily reveals the molecular transformation of ON in penguin guano-affected soil and is important for understanding the N cycle in Antarctica.

Enhanced Uptake of Arsenic Induces Increased Toxicity with Cadmium at Non-Toxic Concentrations on Caenorhabditis elegans.

Cadmium (Cd) and arsenic (As) are widely distributed pollutants that co-exist in the environment; however, their joint toxicity on living organisms is still largely unknown. In this study, we explored the joint toxicity of concurrent exposure to Cd and different As species at low concentrations on Caenorhabditis elegans (C. elegans) in comparison to single exposures. Endpoints such as germ cell apoptosis, the number of oocytes, brood size, and the life span were employed to evaluate the combined effects of Cd and As on exposed C. elegans from L3 or L4 stages. Our results showed that concurrent exposure to non-toxic concentrations of Cd and As caused the synergy of reproductive and developmental toxicity. The presence of Cd promoted the accumulation of As in both germline and intestine detected by laser ablation inductively coupled plasma mass spectrometry (LA-ICP-MS). Although a conversion of As(III) to As(V) was detected as dependent on pH according to the microenvironment of the intestine in the worm, there was no significant difference of toxicity in C. elegans concurrently exposed to Cd and different As species. Using loss-of-function mutant strains, As was deemed responsible for the enhanced joint toxicity, and in which gcs-1 played a key protective role. These data help to better evaluate the comprehensive adverse effects of concurrent exposure of heavy metals at low concentrations on living organisms in the environment.

Spatial distribution of multi-elements in moss revealing heavy metal precipitation in London Island, Svalbard, Arctic.

The Arctic is a sink for major pollutants in the Northern Hemisphere, and is an ideal place to investigate the migration of concerned metals on the local environment. In this study, 13 elements including Li, Ti, V, Cr, Mn, Fe, Co, Cu, Zn, As, Cd, Hg, and Pb were determined in mosses (Dicranum angustum) from London Island in Ny-Ålesund. The results showed that the concentrations of different elements varied greatly at different altitudes, while their distributions in low (0-200 m) and high (200-300 m) altitudes based on cluster analysis were significantly different. Among them, Li, Ti, V, Cr, Mn, Fe, Co, Cu, and As showed significant positive correlations with elevation. This result may be due to the influence of key environmental factors such as elements transported by the airborne dust carried by winds, and surface runoff from snow meltwater. Multiple receptor models (PCA, PMF, and UNMIX) were employed to discuss the sources of metals in mosses from London Island. Elements that showed positive correlation with altitude were attributed to natural sources, and Zn, Cd, Hg, and Pb, which lacked apparent correlation with elevation, were interpreted as from anthropogenic sources by the models. Among them, Zn, Cd, and Hg were from long-range deposition, while Pb was from mixed industrial sources.

Fraction distribution and dynamic cycling of phosphorus in lacustrine sediment at Inexpressible Island, Antarctica.

Phosphorus (P) chemistry and its dynamic cycling are essential for understanding aquatic primary productivity and ecosystem structure. However, there is a lack of knowledge on P chemistry in pristine aquatic ecosystems, such as in Antarctica. Here, we applied the Standards, Measurements and Testing Program (SMT) procedure and nuclear magnetic resonance spectroscopy (NMR) to reveal P speciation in two types of lacustrine sediment cores collected from Inexpressible Island, Ross Sea, East Antarctica. The Positive Matrix Factorization Model and Generalized Additive Models were applied to quantitatively identify the P sources and estimate relative effects of various environmental factors on the speciation. Our results demonstrate that orthophosphate, mainly as Ca-P, is the major component and the ortho-monoesters are the predominant organic phosphorus (OP) form in lacustrine sediments. Ornithogenic lacustrine sediments have a higher content of P as Ca-P than sediments with little or no penguin influence. Our model further suggests that penguin guano is the most important source for Ca-P, accounting for 80%, while detrital input is the predominant source for Fe/Al-P (up to 90%). The content of ortho-monoesters, as revealed by NMR, declines with depth, reflecting mineralization process of OP in the sediments. Moreover, we observed higher relative proportions of organic P in the sediments with little guano influence and the deposition of organic P are likely facilitated by microbial mats. Overall, our data suggest that burial of P in Antarctic lakes is sensitive to different P sources and sedimentary environments. The relatively higher bioavailable phosphorus in lacustrine sediments largely controls growth of aquatic microbial mats in oligotrophic lakes and ponds in Antarctica. The sediment profile data also indicate that P burial increased during the Medieval Climate Anomaly period, and climate warming is more conducive to P burial through the expansion of penguin populations and productivity of microbial mats. Our findings represent the first systematic understanding of natural P cycling dynamics and its main controlling factors in pristine ponds with different organic sources in Antarctica.

Transgenerational reproductive toxicity of 2,4,6-trinitrotoluene (TNT) and its metabolite 4-ADNT in Caenorhabditis elegans.

2,4,6-trinitrotoluene (TNT) as an energetic compound widely used in military applications has aroused great concerns in recent years due to its large-scale contamination in soil and water; however, its toxicity is still largely unknown. In this study, we investigated the reproductive toxicity and the transgenerational effects of TNT on Caenorhabditis elegans (C. elegans). Our data showed that exposure to TNT at concentrations ranging from 10 to 100 ng/mL resulted in decreasing the lifespan, brood size, number of oocytes and eggs in uterus, while increasing the number of germ cell apoptosis in C. elegans. The apoptotic effects of TNT were blocked in mutants of cep-1 (w40), egl-1 (n487), and hus-1 (op241), indicating conserved genotoxic response genes was involved in mediating TNT-induced germ cell apoptosis. Parental exposure to TNT significantly increased the germ cell apoptosis from P0 to F2 generation, but the toxicity faded away in F3 and F4 generations. Furthermore, TNT was rapidly metabolized in P0, and the accumulation of 4-aminodinitrotoluene (4-ADNT), the main metabolite of TNT in C. elegans, showed a significant decrease from P0 to F1 and a slow decrease in the subsequent generations. Our results demonstrated that ingested TNT can cause severe transgenerational reproductive toxicity and be rapidly converted to 4-ADNT in the nematodes. These data provided basis for future studies on the effects of energetic compounds across generations.