Behavioral and biochemical responses of the marine polychaete Perinereis aibuhitensis to 2-ethylhexyl-4-methoxycinnamate (EHMC) exposure.

2-ethylhexyl-4-methoxycinnamate (EHMC) is a commonly used UV filter, and is receiving increasing concerns due to its ubiquitous occurrence in a variety of environmental media and potential adverse effects. This study was aimed to assess the ecotoxicological potentials of EHMC on the marine polychaete Perinereis aibuhitensis. To this end, ragworms were exposed to 2, 20, 200 µg/L EHMC for 14 days and multiple toxicological endpoints were investigated. The results showed that EHMC significantly reduced burrowing rate, but did not affect AChE activity. Exposure to EHMC significantly elevated the activities of SOD and CAT and decreased the levels of lipid peroxidation. Besides, the induction of AKP activity indicated a stimulated immune response in the ragworms when exposed to high concentration of EHMC. Furthermore, the upregulated expression of caspase-8 suggested that EHMC might induce apoptosis in ragworms via the death receptor-mediated extrinsic pathway. Our findings highlight the potential environmental risks of EHMC to marine ecosystems.

Uptake and toxicity of micro-/nanoplastics derived from naturally weathered disposable face masks in developing zebrafish: Impact of COVID-19 pandemic on aquatic life.

The unprecedented proliferation of disposable face masks during the COVID-19 pandemic, coupled with their improper disposal, threatens to exacerbate the already concerning issue of plastic pollution. This study evaluates the role of environmentally weathered masks as potential sources of microplastics (MPs) and nanoplastics (NPs) and assesses their adverse impact on the early life stages of zebrafish. Experimental findings revealed that a single disposable mask could release approximately 1.79 × 109 particles, with nearly 70% measuring less than 1 µm, following 60 days of sunlight exposure and subsequent sand-induced physical abrasion. Remarkably, the MPs/NPs (MNPs) emanating from face masks have the potential to permeate the outer layer (chorion) of zebrafish embryos. Furthermore, due to their minute size, these particles can be consumed by the larvae's digestive system and subsequently circulated to other tissues, including the brain. Exposure to mask-derived MNPs at concentrations of 1 and 10 µg/L led to significant cases of developmental toxicity, incited oxidative stress, and prompted cell apoptosis. A subsequent metabolomics analysis indicated that the accumulation of these plastic particles perturbed metabolic functions in zebrafish larvae, primarily disrupting amino acid and lipid metabolism. The outcomes of this research underscore the accelerating possibility of environmental aging processes and physical abrasion in the release of MNPs from disposable face masks. Most importantly, these results shed light on the possible ecotoxicological risk posed by improperly disposed of face masks.

Environmentally relevant concentrations of tris (2-chloroethyl) phosphate (TCEP) induce hepatotoxicity in zebrafish (Danio rerio): a whole life-cycle assessment.

Tris (2-chloroethyl) phosphate (TCEP), a typical organophosphate flame retardant, is of increasingly great concern considering their ubiquitous presence in aquatic environments and potential ecotoxicity. The present work was aimed to investigate the potential growth inhibition and hepatic stress induced by whole life-cycle exposure to TCEP (0.8, 4, 20 and 100 µg/L) in zebrafish. The results revealed that the body length, body mass and hepatic-somatic index (HSI) of zebrafish were significantly declined after exposure to TCEP for 120 days. GPx activity and GSH content were increased in the liver of zebrafish treated with low concentrations (0.8 and 4 µg/L) of TCEP, while exposure to high concentrations (20 and 100 µg/L) of TCEP reduced antioxidative capacity and elevated lipid peroxidation (LPO) levels. Gene transcription analysis demonstrated that the mRNA levels of nrf2 were altered in a similar manner to the transcription of the downstream genes nqo1 and hmox1, suggesting that Nrf2-Keap1 pathway mediated TCEP-induced oxidative stress in zebrafish liver. In addition, TCEP exposure might alleviate inflammatory response through down-regulating transcription of inflammatory cytokines (il-1ß, il-6 and inos), and induce apoptosis via activating the p53-Bax pathway. Moreover, whole life-cycle exposure to TCEP caused a series of histopathological anomalies in zebrafish liver. Overall, our results revealed that lifetime exposure to environmentally relevant concentrations of TCEP could result in growth retardation and induce significant hepatotoxicity in zebrafish.

Life-cycle exposure to tris (2-chloroethyl) phosphate (TCEP) causes alterations in antioxidative status, ion regulation and histology of zebrafish gills.

Tris (2-chloroethyl) phosphate (TCEP) has been receiving great concerns owing to its ubiquitous occurrence in various environmental compartments and potential risks to wildlife and humans. Gill is structural basis for ion regulation and homeostasis in fish and susceptible to xenobiotics. However, current knowledge on the impacts of long-term exposure to TCEP on the structure and physiological function of fish gills are insufficient. In this work, zebrafish were exposed to environmental realistic concentrations (0.8, 4, 20 and 100 µg/L) of TCEP from 3 h post ferterlization (hpf) till 120 days post ferterlization (dpf). Our results demonstrated that life-cycle exposure to TCEP significantly decreased the activity of glutathione S-transferase (GST), but elevated the activities of antioxidative enzymes including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and increased malondialdehyde (MDA) content in zebrafish gills. Gene transcription analysis implied that the mRNA expressions of antioxidant-related genes (nrf2, cat and nqo1) were induced, while the transcription of gstα1, hmox1, keap1 were down-regulated, indicating that Nrf2-Keap1 pathway might be activated to defend the oxidative stress induced by TCEP. Additionally, the ion homeostasis was disrupted by TCEP exposure, evidenced by reduced activities of Na+/K+-ATPase (NKA), Ca2+-ATPase and Mg2+-ATPase and downregulated transcription levels of ncc, nkcc, cftr and clc-3. Besides, whole-life exposure to TCEP resulted in a series of structural damages to gills, including epithelial lifting, epithelial rupture, telangiectasis, vacuolation, edema and shortened gill lamellae. Overall, our results demonstrated that long-term TCEP exposure could induce oxidative stress, affect ion regulation and cause histological changes in zebrafish gills.

A multibiomarker approach to assess the ecotoxicological effects of diclofenac on Asian clam Corbicula fluminea (O. F. Müller, 1774).

Diclofenac (DCF), one of the most current and widely used nonsteroidal anti-inflammatory drugs (NSAIDs), has been frequently detected in aquatic environments worldwide. However, the ecotoxicological effects of DCF on freshwater invertebrates remain largely unknown. In the present study, Corbicula fluminea were exposed to environmentally relevant concentrations of DCF (0, 2, 20, and 200 µg/L) for 28 days, and the potential adverse effects of DCF on siphoning behavior, antioxidant responses, and apoptosis were investigated. Our results showed that the siphon efficiencies of clams were significantly suppressed under DCF stress. DCF exerted neurotoxicity via reducing the activity of acetylcholinesterase (AChE) in gills and digestive gland of C. fluminea. Exposure to DCF induced antioxidant stress and increased malondialdehyde (MDA) levels in both gills and digestive gland of C. fluminea. Transcriptional alterations of apoptosis-related genes indicated that DCF might induce apoptosis by triggering mitochondrial apoptotic pathway. These findings can improve our understanding of the ecological risk of DCF in freshwater ecosystems.

Comparative transcriptome analysis reveals immunotoxicology induced by three organic UV filters in Manila clam (Ruditapes philippinarum).

Benzophenone-3 (BP-3), 4-methyl-benzylidene camphor (4-MBC) and 2-ethyl-hexyl-4-trimethoxycinnamate (EHMC) are commonly used organic ultraviolet (UV) filters and are frequently detected in water environments. In the present study, we studied the potential adverse impacts of UV filter exposures in Ruditapes philippinarum by investigating transcriptomic profiles and non-specific immune enzyme activities. Transcriptome analysis showed that more genes were differentially regulated in EHMC-treated group, and down-regulated genes (2009) were significantly more than up-regulated ones (410) at day 7. Function annotation revealed that pathways "immune system", "cell growth and death" and "infectious diseases" were significantly enriched. Generally, combined qPCR and biochemical analyses demonstrated that short-term exposure to low dose of UV filters could activate immune responses, whereas the immune system would be restrained after prolonged exposure. Taken together, the present study firstly demonstrated the immunotoxicology induced by BP-3, 4-MBC and EHMC on R. philippinarum, indicating their potential threats to the survival of marine bivalves.

Parental whole life-cycle exposure to tris (2-chloroethyl) phosphate (TCEP) disrupts embryonic development and thyroid system in zebrafish offspring.

Tris (2-chloroethyl) phosphate (TCEP), an emerging environmental pollutant, has been frequently detected in natural waters. The objective of this study was to investigate possible parental transfer of TCEP and transgenerational effects on the early development and thyroid hormone homeostasis in F1 larvae following parental whole life-cycle exposure to TCEP. To this end, zebrafish (Danio rerio) embryos were exposed to environmentally relevant concentrations (0.8, 4, 20 and 100 µg/L) of TCEP for 120 days until sexual maturation. Parental exposure to TCEP resulted in significant levels of TCEP, developmental toxicity including decreased survival and final hatching rates, accelerated heart rate and elevated malformation rate, as well as induction of oxidative stress and cell apoptosis in F1 offspring. In F1 eggs, declined thyroxin (T4) levels were observed, consistent with those in plasma of F0 adult females, indicating the maternal transfer of thyroid endocrine disruption to the offspring. In addition, mRNA levels of several genes along the hypothalamic-pituitary-thyroid (HPT) axis were significantly modified in F1 larvae, which could be linked to transgenerational developmental toxicity and thyroid hormone disruption. For the first time, we revealed that the parental exposure to environmentally relevant levels of TCEP could cause developmental toxicity and thyroid endocrine disruption in subsequent unexposed generation.

Decreased Salinity Offsets the Stimulation of Elevated pCO2 on Photosynthesis and Synergistically Inhibits the Growth of Juvenile Sporophyte of Saccharina japonica (Laminariaceae, Phaeophyta).

The combined effect of elevated pCO2 (Partial Pressure of Carbon Dioxide) and decreased salinity, which is mainly caused by freshwater input, on the growth and physiological traits of algae has been poorly assessed. In order to investigate their individual and interactive effects on the development of commercially farmed algae, the juvenile sporophytes of Saccharina japonica were cultivated under different levels of salinity (30, 25 and 20 psu) and pCO2 (400 and 1000 µatm). Individually, decreased salinity significantly reduced the growth rate and pigments of S. japonica, indicating that the alga was low-salinity stressed. The maximum quantum yield, Fv/Fm, declined at low salinities independent of pCO2, suggesting that the hyposalinity showed the main effect. Unexpectedly, the higher pCO2 enhanced the maximum relative electron transport rate (rETRmax) but decreased the growth rate, pigments and soluble carbohydrates contents. This implies a decoupling between the photosynthesis and growth of this alga, which may be linked to an energetic reallocation among the different metabolic processes. Interactively and previously untested, the decreased salinity offset the improvement of rETRmax and aggravated the declines of growth rate and pigment content caused by the elevated pCO2. These behaviors could be associated with the additionally decreased pH that was induced by the low salinity. Our data, therefore, unveils that the decreased salinity may increase the risks of future CO2-induced ocean acidification on the production of S. japonica.

The physiological, biochemical and transcriptional responses to sulfamethoxazole in the Asian clam, Corbicula fluminea (O. F. Müller, 1774).

Sulfamethoxazole (SMX), a broad-spectrum antibiotic, has been widely used in the treatment and prevention of infection caused by bacteria in recent years. The present study was aimed to evaluate the response mechanisms to SMX stress in gills and digestive gland of Corbicula fluminea (O. F. Müller, 1774). To this end, clams were exposed to environmentally relevant concentrations of SMX (0, 1, 10 and 100 µg/L) for 7 and 28 days, and siphon behavior, tissue-specific enzymatic and transcriptional changes were assayed. Our results showed that exposure to SMX significantly suppressed filtration rate and acetylcholinesterase (AChE) activity, activated antioxidant defense system and elevated transcription of several genes related to cell apoptosis in gills and digestive gland of clams. In general, SMX at environmentally relevant concentrations exhibited a negative impact on siphon behavior and induced neurotoxicology, oxidative stress and cell apoptosis in C. fluminea. The current study will help broaden our understanding of the ecotoxicity of SMX on freshwater bivalves.

Insights into the mechanisms of tris(2-chloroethyl) phosphate-induced growth inhibition in juvenile yellow catfish Pelteobagrus fulvidraco.

With the gradual elimination of brominated flame retardants (BFRs), the production and application of tris (2-chloroethyl) phosphate (TCEP), as a substitute of BFRs, has increased greatly. The objective of the present study was to comprehensively explore the potential adverse effects of TCEP on fish growth and the possible underlying mechanisms. To this end, juvenile yellow catfish (Pelteobagrus fulvidraco) were exposed to environmentally relevant concentrations of TCEP (0, 1, 10 and 100 µg/L) for 30 days. The results showed that exposure to high concentrations of TCEP (10 and 100 µg/L) significantly decreased body weight, body length and specific growth rate (SGR). Plasma IGF-I levels and hepatic mRNA levels of igf1 and igf1r were all reduced, while the transcriptional levels of IGFBPs (igfbp2, igfbp3, igfbp5) were significantly up-regulated in the liver of yellow catfish under exposure to 10 and 100 µg/L TCEP. TCEP-induced growth inhibition might be related to somatostatin (SS) signaling system, as evidenced by elevated mRNA transcriptions of ss in brain and its receptors (sstr2, sstr3, sstr5) in liver. In addition, fish exposed to high concentrations of TCEP displayed multiple histological alterations in liver. Taken together, these findings suggested that TCEP (>10 µg/L) might exert its inhibitory effect on fish growth through interfering with the GH/IGF axis and SS signaling system, and by impairing hepatic structures.

Exposure to diclofenac alters thyroid hormone levels and transcription of genes involved in the hypothalamic-pituitary-thyroid axis in zebrafish embryos/larvae.

Diclofenac (DCF), one of typical non-steroidal anti-inflammatory drugs (NSAIDs), has been frequently detected in various environmental media. Nevertheless，the potential endocrine disrupting effects of DCF on fish were poorly understood. In the present study, zebrafish embryos/larvae were used as a model to evaluate the adverse effects of DCF on development and thyroid system. The results demonstrated that DCF only significantly decreased the heart rate at 72 h post-fertilization (hpf), exhibiting limited influence on the embryonic development of zebrafish. Treatment with DCF significantly reduced whole-body thyroxine (T4) levels, and changed transcriptional levels of several genes related to the hypothalamic-pituitary-thyroid (HPT) axis. These findings provide important information regarding to the mechanisms of DCF-induced developmental toxicity and thyroid disruption in fish.

Effects of long-term cadmium exposure on growth, antioxidant defense and DNA methylation in juvenile Nile tilapia (Oreochromis niloticus).

Cadmium (Cd) is a ubiquitous environmental contaminant, posing serious threats to aquatic organisms. The aims of the present study were to investigate the effects of long-term Cd exposure on the growth, GH/IGF axis, antioxidant defense and DNA methylation in juvenile Nile tilapia (Oreochromis niloticus). To this end, juvenile Nile tilapia were exposed to 0, 10 and 50 µg∙L-1 Cd for 45 and 90 days. The obtained results revealed that exposure to high concentrations of Cd significantly decreased body mass and body length, and down-regulated mRNA levels of GHRs, IGF-I and IGF-II in the liver of Nile tilapia. Cd exposure induced oxidative stress including the reduction of antioxidant activities and increases of malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) contents. Beside, the global DNA methylation levels significantly decreased with increasing Cd concentration and exposure time, which might result from increased oxidative DNA damage, the down-regulated expression of DNMT3a and DNMT3b and up-regulated expression of TET1 and TET2. In conclusion, long-term Cd exposure could inhibit growth, reduce antioxidant capacity and lead to oxidative damages to lipid and DNA, and decrease global DNA methylation level in juvenile Nile tilapia.

Effects of tris (2-chloroethyl) phosphate (TCEP) on survival, growth, histological changes and gene expressions in juvenile yellow catfish Pelteobagrus fulvidraco.

Tris (2-chloroethyl) phosphate (TCEP) is an emerging aquatic environmental pollutant. In the present study, juvenile yellow catfish (Pelteobagrus fulvidraco) were exposed to environmentally relevant concentrations of TCEP for 30 days. The results showed that TCEP exposure decreased the survival rate (100 µg/L), body weight (10 and 100 µg/L) and specific growth rate (10 and 100 µg/L) of juvenile yellow catfish. Exposure to TCEP resulted in pronounced damages of gill structures. Gene transcription analysis showed that the antioxidant capacity of the liver and gills was affected; CYP1A1 might contribute to phase I metabolism of TCEP in the liver rather than CYP1B1; TCEP stress might increase the demand of ion transport in fish gill; TCEP could stimulate the immune response and might induce apoptosis via a p53-Bax pathway and caspase-dependent pathway in gills. Collectively, these findings provide new insights into the toxic effects of TCEP on fish.

Effects of environmentally relevant concentrations of tris (2-chloroethyl) phosphate (TCEP) on early life stages of zebrafish (Danio rerio).

Tris (2-chloroethyl) phosphate (TCEP) has been received great concerns because of its increasing presence in various environmental compartments and toxicity. In the present study, zebrafish embryos were exposed to environmentally relevant concentrations of TCEP (0.2, 2, 20, 200 µg/L) from 3 to 120 h post-fertilization (hpf). The results showed that TCEP exposure (20, 200 µg/L) led to developmental toxicity including decreased body length and delay of hatching. Treatment with TCEP significantly decreased whole-body thyroxine (T4) levels and mRNA level of thyroglobulin (tg), and enhanced transcriptions of genes sodium/iodide symporter (nis), thyroid hormone receptor α (trα) and ugt1ab involved in thyroid synthesis and metabolism, respectively. Additionally, TCEP altered the transcription of α1-tubulin, gap43 and mbp related to nervous system development, even at relatively low concentrations. Overall, our results revealed that TCEP exposure can lead to developmental toxicity, thyroid endocrine disruption and neurotoxicity on early developmental stages of zebrafish.

Bioaccumulation and oxidative damage of polycyclic aromatic hydrocarbon mixtures in Manila clam Ruditapes philippinarum.

The aim of this study was to investigate the bioaccumulation and oxidative damage of Manila clam, Ruditapes philippinarum, exposed to four selected mixtures of polycyclic aromatic hydrocarbons (PAHs; benzo (a) pyrene (BaP), benzo (a) anthracene (BaA), benzo (b) fluoranthene (BbF), and chrysene (Chr) in equal proportion. For this purpose, clams were exposed to PAHs (BaP:BbF:BaA:Chr = 1:1:1:1) at different concentrations (0.05, 0.5, and 5 µg/L) for 21 days, followed by a 15-day depuration period. All four PAHs accumulated in the gill, digestive gland, adductor muscle, and soft tissue of Manila clams, and all PAH treatment groups showed clear time and dose dependence. The decreasing order of bioaccumulation for the four PAHs in the exposure experiment was Chr > BaA > BaP > BbF. Moreover, the order of PAH bioaccumulation for the four tissues during the whole experiment was digestive gland > gill > soft tissues > adductor muscles. Although the initial concentrations of the four PAHs were the same, the final accumulated contents were different. Therefore, we also determined the detoxification processes of the four PAH mixtures in gills and digestive glands. The bioaccumulation of Chr was higher than the other three PAHs, probably because clams have a lower metabolic capacity for Chr than for BaP, BbF, and BaA. Exposure to PAH mixtures can result in oxidative damage, as indicated by the fact that DNA strand breaks, lipid peroxidation (LPO), and protein carbonyl (PC) were induced significantly (P < 0.05), except in the low-dose groups of PAHs, and different trends were detected with time of exposure. According to the correlation analysis, aryl hydrocarbon hydroxylase, glutathione s-transferase, superoxide dismutase, DNA strand break, PC, and LPO in both the gill and digestive gland are potential early indicators of PAH mixtures. We investigated the accumulation rules of R. philippinarum exposed to the selected PAHs and screened the potential biomarkers. The results of our study provide important scientific information for the purpose of monitoring marine pollution.

Effect of air pre-exposure on Tetrabromobisphenol A resistance in the clam Ruditapes philippinarum.

The present study was conducted to evaluate how air pre-exposure influences the responses in gills and digestive gland of Ruditapes philippinarum on subsequent Tetrabromobisphenol A (TBBPA) exposure. Firstly, clams were maintained in seawater or pre-exposed to air for 24 h, and then exposed to 0 or 100 µg/L TBBPA. Clam tissues were sampled after 1 day (T1) and 7 days (T7) of exposure to TBBPA. The results showed that in comparison with TBBPA exposure alone, air pre-exposure following TBBPA exposure reduced TBBPA accumulation in both tissues, up-regulated mRNA levels of CAT, Hsp70 and pi-GST in gills, and induced GST activity and P-glycoprotein (Pgp) mRNA level in digestive gland of clams at T1, whereas increased lipid peroxidation at T7. Overall, the findings indicate that 24-h exposure to air can activate a priming mechanism withstanding the subsequent TBBPA exposure, which is transient and may change after prolonged subsequent exposure.

Bioaccumulation and detoxification responses in the scallop Chlamys farreri exposed to tetrabromobisphenol A (TBBPA).

Tetrabromobisphenol A (TBBPA) is currently the most widely used brominated flame retardant (BFR). In this study, the bioaccumulation of TBBPA and its consequent detoxification responses were examined in the scallop Chlamys farreri over 10 days' exposure. Chemical analysis showed that C. farreri absorbed TBBPA rapidly and an approximate steady state was achieved within 6 days. The mRNA expression levels of three important genes involved in aryl hydrocarbon receptor (AhR) pathway were down-regulated upon TBBPA exposure. Both CYP3A and CYP4 showed time-dependent responses to TBBPA exposure. Glutathione-S-transferase (GST) activity and gene expression level, and UDP-glucuronosyltransferase (UGT) activity were increased in time- and dose-dependent manners, confirming their role in the phase II metabolism of TBBPA. The TBBPA-elicited down-regulation of the P-glycoprotein (Pgp) gene was observed in all treatments. This study provides a preliminary basis for studying TBBPA detoxification mechanisms of marine bivalves.

Exposure of Chlamys farreri to tetrabromobisphenol A: accumulation and multibiomarker responses.

Tetrabromobisphenol A (TBBPA) is currently the most widely used brominated flame retardant (BFR). To date, the toxic effects of TBBPA remains poorly understood in aquatic organisms, especially in bivalves. The objective of this experiment was to examine bioaccumulation and multibiomarker responses in the scallop Chlamys farreri exposed to TBBPA under laboratory conditions. The results showed that TBBPA was rapidly accumulated in and then eliminated from the gill and digestive gland of the scallops. TBBPA exposure invoked alterations in the detoxification system and induced oxidant stress and biomacromolecule damages in the gill and digestive gland of C. farreri. Additionally, glutathione-S-transferase (GST) activity, lipid peroxidation (LPO) level, cytochrome b5 (Cyt b5) content, and DNA strand break had good correlations with TBBPA accumulation levels in the gill and digestive gland of C. farreri. Summarizing, these results enabled us to hypothesize several toxic mechanisms of TBBPA and select potential biomarkers for TBBPA pollution monitoring.

Deep sequencing of the scallop Chlamys farreri transcriptome response to tetrabromobisphenol A (TBBPA) stress.

Tetrabromobisphenol-A (TBBPA) is currently the most widely used brominated flame retardant (BFR) and has been proven to have a very high toxicity to aquatic organisms including bivalves. However, molecular responses to TBBPA in bivalve remain largely unknown. Novel high-throughput deep sequencing technology has been a powerful tool for looking at molecular responses to toxicological stressors in organisms. Using Illumina's digital gene expression (DGE) system, we investigated TBBPA-induced transcriptome response in the digestive gland tissue of scallop Chlamys farreri. In total, 173 and 266 genes were identified as significantly up- or down-regulated, respectively. Functional analysis based on gene ontology (GO) classification system and Kyoto Encyclopedia of Genes and Genomes (KEGG) database revealed that TBBPA significantly altered the expression of genes involved in stress response, detoxification, antioxidation, and innate immunity which were extensively discussed. In particular, evidence for the endocrine disrupting effect of TBBPA on bivalve was first obtained in this study. Quantitative real-time PCR was performed to ascertain the mRNA expression of several genes identified by the DGE analysis. The results of this study may serve as a basis for future research on molecular mechanism of toxic effects of TBBPA on marine bivalves.

Dietary accumulation of tetrabromobisphenol A and its effects on the scallop Chlamys farreri.

Tetrabromobisphenol A (TBBPA) is currently the most widely-used brominated flame retardant (BFR) and has been proven to have a very high toxicity to aquatic organisms including bivalves. In this study, a laboratory experiment was conducted to obtain a better understanding of the role of algae food on the bioaccumulation of TBBPA and its effects on the suspension-feeding bivalve, the scallop, Chlamys farreri. Scallops were exposed to TBBPA via algae food alone or food+water for 10 days. Results showed that TBBPA was accumulated rapidly by scallops, reaching an approximate steady state in soft tissues within 3 days. The primary route of TBBPA accumulation was via the water, while dietary uptake was relatively minor. TBBPA exposure led to significant inhibition on microsomal cytochrome P450 and cytochrome b5 levels in gills and digestive gland, whereas GST activity and GSH level increased significantly, which indicated that TBBPA could be a suitable substrate to directly participate in phase II metabolism. TBBPA clearly induced the activity of SOD, suggesting the oxidant stress induced by TBBPA. This study suggests that dietary uptake was not the predominant uptake route for TBBPA in bivalves and also provides a preliminary basis for studying the detoxification and antioxidant responses of marine bivalves upon exposure to TBBPA.