Triphenyltin Research Articles

Toxic Effects of Tributyltin, Triphenyltin, and SnCl2 on the Development of Zebrafish (Danio rerio) Embryos

ABSTRACTTin (Sn) is one of the heavy metals to which various functions in biological development are attributed in small quantities, for example, a role in cell structure, enzyme activities, and protein and carbohydrate metabolism in fish. Tributyltin (TBT) and triphenyltin (TPT) are endocrine disrupting chemicals that are widely distributed in the aquatic environment. The aim of this study was to investigate the effects of TBT, TPT, and SnCl2 on the embryonic development of zebrafish. In this study, zebrafish embryos were used to observe the acute toxicity of TBT, TPT, and SnCl2. Fish embryo toxicity analysis was performed for different TBT, TPT, and SnCl2 concentrations (1, 5, 10, 15, and 20 ng/L). Fertilized eggs in 24‐well plates (20 eggs in each concentration) were incubated at 26°C for 4 days, and embryo clotting, embryo heartbeat, and morphological abnormalities were recorded after 96 h. Coagulation increased significantly in a dose‐dependent manner, and TBT was able to induce coagulation in zebrafish embryos. Heartbeat changes significantly decreased (p < 0.05) in a dose‐dependent manner at different TBT doses (p < 0.05). The percentage of mortality was higher in embryos at trace levels of TBT, indicating that the embryos are more sensitive to the toxicity of TBT. TBT is therefore extremely toxic and can have fatal consequences for zebrafish embryos, ultimately leading to the extinction of species and a decline in biodiversity in the aquatic environment. After analyzing the images 96 h after fertilization and converting them to a teratogenic index score, it was found that the index for the two compounds TPT and TBT was 4.6 and 9.6 ng/L, respectively.

Protective Role of Sulforaphane against Physiological Toxicity of Triphenyltin in Common Carp (Cyprinus carpio haematopterus).

This experiment mainly explored the protective role of sulforaphane (SFN) against physiological toxicity of triphenyltin (TPT) in Cyprinus carpio haematopterus. In total, 320 Fish (56.90 ± 0.40 g) were randomly divided into four groups with four replicates each. The control group was fed the basal diet, the TPT group (TPT) was exposed to 10 ng L-1 TPT on the basis of the control group, the SFN + TPT group (TPT + SFN) was fed a diet supplemented with 10 mg kg-1 SFN on the TPT group, and the SFN group (SFN) was fed a diet supplemented with 10 mg kg-1 SFN. After 56 days of breeding trials, the results showed that TPT exposure resulted in a remarkable decrease (p < 0.05) in final weight, weight gain rate (WGR), specific growth rate (SGR), and condition factor (CF), but an increase (p < 0.05) in feed conversion ratio (FCR) and hepatosomatic index (HSI) of fish. TPT treatment decreased (p < 0.05) the amounts of hematocrit (Hct) and hemoglobin (Hb), plasma complement component 3 (C3) and C4 contents, alternative complement pathway (ACH50), acid phosphatase (ACP) and lysozyme (LZM) activities, liver glutathione (GSH) content, catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPX) activities, interleukin 10 (IL-10), and SOD mRNA expressions, but increased (p < 0.05) plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities, liver malonaldehyde (MDA) content, tumor Cyclooxygenase 2 (COX2), and necrosis factor α (TNFα), IL-1β, and MDA mRNA expressions. A histological analysis of the liver showed that a higher occurrence rates of the hepatocyte hypertrophy, nuclear disappearance and hepatocyte vacuolization was observed in the hepatocytes of fish exposed to TPT, and it was accompanied by the dilation of hepatic sinusoids. In addition, the toxicity induced by TPT was significantly improved in the groups that were treated with SFN, and SFN was able to improve growth performance and immunity, alleviate TPT-induced changes in inflammatory factors, ameliorate oxidative stress, and increase the activity of antioxidant enzymes (p < 0.05). The addition of SFN also alleviated liver damage caused by TPT and protected the structural integrity of the liver. Overall, these findings suggest that TPT inhibited the growth, immunity, and antioxidant capacity of Cyprinus carpio haematopteru. Dietary SFN could be beneficial for growth promotion, immunity, antioxidant capacity, and protection of liver structural integrity. Therefore, SFN is a prospective feed supplement for ameliorating the damage caused to fish by TPT contamination.

Green and sensitive method combining ultrasonic solvent extraction, stir bar sorptive extraction and thermal desorption-gas chromatography–tandem mass spectrometry for determination of organotin compounds in sediment

A method integrating ultrasonic solvent extraction (USE) and stir bar sorptive extraction (SBSE) with thermal desorption-gas chromatography–tandem mass spectrometry (TD-GC–MS/MS) was developed and validated for determining critical organotin compounds (OTCs)—tributyltin (TBT) and triphenyltin (TPhT)—in sediment. In preparing a 0.5 g sediment sample, two 1-min cycles of US bath solvent extraction (using equal parts CH3COOH and MeOH), were followed by derivatization with NaBEt4 in the presence of a methanolic-aqueous solution of CH3COONa and SBSE for 1 h, achieving analyte recoveries of 64–94 %. Matrix-matched internal standard calibration and the use of an isotopically labelled recovery standard corrected for analyte losses and matrix effect (ME), ensuring accurate results for triorganotins. However, the method was not suitable for mono- and diorganotins due to low and anomalous recoveries caused by ME. Miniaturizing and optimizing the sample preparation reduced chemicals use and waste, contributing to the method being deemed ’an excellent green analysis’ by the Analytical Eco-Scale assessment. The method achieved a limit of quantification (LOQ) of 0.081 ng g−1 and an expanded uncertainty (U) value of 15 % for TBT, meeting the environmental quality standards (EQS) criteria of the European Union Water Framework Directive. Its applicability was demonstrated through the analysis of actual sediment samples and natural matrix certified reference materials.

TPT disrupts early embryonic development and glucose metabolism of marine medaka in different salinites

Triphenyltin (TPT) is an organotin compound frequently detected in coastal estuaries, yet studies on TPT's effects in regions with significant salinity fluctuations, such as coastal estuaries, are currently limited. To investigate the toxic effects of TPT under different salinity conditions, this study focused on marine medaka (Oryzias melastigma) embryos. Through early morphological observations, RNA-seq analysis, biochemical marker assays, and qPCR detection, we explored the impact of TPT exposure on the early embryonic development of marine medaka under varying salinities. The study found that TPT exposure significantly increased embryo mortality at salinities of 0 ppt and 30 ppt. RNA-seq analysis revealed that TPT primarily affects glucose metabolism and glycogen synthesis processes in embryos. Under high salinity conditions, TPT may inhibit glucose metabolism by suppressing glycolysis and promoting gluconeogenesis. Furthermore, TPT exposure under different salinities led to the downregulation of genes associated with the insulin signaling pathway (ins, insra, irs2b, pik3ca, pdk1b, akt1, foxo1a), which may be linked to suppressed glucose metabolism and increased embryonic mortality. In summary, TPT exposure under different salinities affects the early development of marine medaka embryos and inhibits glucose metabolism. This study provides additional data to support research on organotin compounds in coastal estuaries.

Sulforaphane modulates some stress parameters in TPT-exposed Cyprinus carpio in relation to liver metabolome

This study aimed to investigate the protective effect of sulforaphane (SFN) on liver injury induced by triphenyltin (TPT) in Cyprinus carpio (C. carpio). The fish (average weight of 56.9±0.4 g) were divided into 4 groups with four replicates: the control, TPT, SFN+TPT and SFN groups. Twenty fish were selected from each tank and cultured for 8 weeks. Then, serum and liver samples were collected for physiological, biochemical and metabolomic analyses. In the present study, TPT downregulated the expression of the lysozyme gene, upregulated HSP70 and Hsp90 gene expression, and decreased the activities of serum antioxidant enzymes (SOD, CAT, and GPX). However, dietary SFN alleviated oxidative stress, and prevented changes in immune genes. Metabolomic analysis revealed that TPT exposure changed key metabolites in the main phenylalanine, fatty acid and glycerophosphatide metabolic pathways, which are related to inflammation, oxidative stress and immunity and might also lead to an imbalance of liver energy and lipid metabolism. Dietary SFN promoted amino acid metabolism and increased metabolites related to immunity, anti-inflammation, antioxidation, and protein synthesis in liver of C. carpio. In summary, dietary SFN supplementation reversed TPT-induced decreases in immunity and oxidative stress and regulated amino acid metabolism, lipid metabolism, inflammation and immunity-related metabolic pathways.

Neurobehavioral toxicity induced by combined exposure of micro/nanoplastics and triphenyltin in marine medaka (Oryzias melastigma)

Microplastics/nanoplastics (MNPs) inevitably coexist with other pollutants in the natural environment, making it crucial to study the interactions between MNPs and other pollutants as well as their combined toxic effects. In this study, we investigated neurotoxicity in marine medaka (Oryzias melastigma) exposed to polystyrene micro/nanoplastics (PS-MNPs), triphenyltin (TPT), and PS-MNPs + TPT from physiological, behavioral, biochemical, and genetic perspectives. The results showed that marine medaka exposed to 200 ng/L TPT or 200 μg/L PS-NPs alone exhibited some degree of neurodevelopmental deficit, albeit with no significant behavioral abnormalities observed. However, in the PS-MP single exposure group, the average acceleration of short-term behavioral indices was significantly increased by 78.81%, indicating a highly stress-responsive locomotor pattern exhibited by marine medaka. After exposure to PS-MNPs + TPT, the swimming ability of marine medaka significantly decreased. In addition, PS-MNPs + TPT exposure disrupted normal neural excitability as well as activated detoxification processes in marine medaka larvae. Notably, changes in neural-related genes suggested that combined exposure to PS-MNPs and TPT significantly increased the neurotoxic effects observed with exposure to PS-MNPs or TPT alone. Furthermore, compared to the PS-MPs + TPT group, PS-NPs + TPT significantly inhibited swimming behavior and thus exacerbated the neurotoxicity. Interestingly, the neurotoxicity of PS-MPs was more pronounced than that of PS-NPs in the exposure group alone. However, the addition of TPT significantly enhanced the neurotoxicity of PS-NPs compared to PS-MPs + TPT. Overall, the study underscores the combined neurotoxic effects of MNPs and TPT, providing in-depth insights into the ecotoxicological implications of MNPs coexisting with pollutants and furnishing comprehensive data.

Abnormal eyes and spine development in zebrafish (Danio rerio) embryos and larvae induced by triphenyltin

Triphenyltin (TPT) is widely used in crop pest control and ship antifouling coatings, which leads to its entry into aquatic environment and poses a threat to aquatic organisms. However, the effects of TPT on the early life stages of wild fish in natural water environments remains unclear. The aim of this study was to assess the toxic effects of TPT on the early life stages of fish under two different environments: field investigation and laboratory experiment. The occurrence of deformities in wild fish embryos and larvae in the Three Gorges Reservoir (TGR) and the developmental toxicity of TPT at different concentrations (0, 0.15, 1.5 and 15 μg Sn/L) to zebrafish embryos and larvae were observed. The results showed that TPT content was higher in wild larvae, reaching 27.21 ng Sn/g w, and the malformation of wild fish larvae mainly occurred in the eyes and spine under natural water environment. Controlled experiment exposure of zebrafish larvae to TPT also resulted in eye and spinal deformities. Gene expression analysis showed that compared with the control group, the expression levels of genes related to eye development (sox2, otx2, stra6 and rx1) and spine development (sox9a and bmp2b) were significantly up-regulated in the 15 μg Sn/L exposure group, which may be the main cause of eye and spine deformity in the early development stage of fish. In addition, the molecular docking results further elucidate that the strong hydrophobic and electrostatic interactions between TPT and protein residues are the main mechanism of TPT induced abnormal gene expression. Based on these results, it can be inferred that TPT is one of the teratogenic factors of abnormal eye and spine development in the early life stage of fish in the TGR. These findings have important implications for understanding the toxicity of TPT on fish.

Triphenyltin(IV) compounds bearing modulated azo-carboxylato ligands: Synthesis, structural characterization, in vitro cytotoxicity, BSA/DNA binding affinity, and in silico studies

Three novel triphenyltin(IV) compounds with modulated azo-carboxylato ligands: triphenylstannyl (E)-4-((2-hydroxynaphthalen-1-yl)diazenyl)benzoate, 1, triphenylstannyl (E)-4-((4-hydroxyphenyl)diazenyl)benzoate, 2, and triphenylstannyl (E)-4-((4-(dimethylamino)phenyl)diazenyl)benzoate, 3, were synthesized and characterized by elemental analysis, FTIR and NMR (1H, 13C, 119Sn) spectroscopy. The structures and spectra of compounds were predicted by Density Functional Theory (DFT) methods at B3LYP-D3BJ/6–311++G(d,p)(H,C,N,O)/LanL2DZ(Sn) level of theory. Furthermore, the antitumor potential of ligand precursors, HL1–HL3, and appropriate organotin(IV) compounds 1–3 was evaluated across mouse melanoma B16F1, human breast adenocarcinoma MCF-7, human colorectal HT-29 and human prostate PC3 cell lines using MTT and CV assays. The organotin(IV) compounds exhibit enhanced cellular uptake and efficacy in reducing viable cell numbers when compared to free acids. Specifically, compound 3 demonstrates a notable impact at lower nanomolar concentrations on all tested cell lines. Moreover, 3 induces cell death in MCF-7 cells by inhibiting cell division and promoting the overproduction of cellular nitric oxide (NO), ultimately leading to caspase-independent apoptosis. Importantly, this process occurs without concurrent activation of autophagy or the generation of ROS/RNS species. The binding affinity of 1–3 with calf thymus DNA (CT-DNA) and bovine serum albumin (BSA) was investigated by fluorescence spectroscopy and molecular docking simulations, suggesting their capacity to interact with these biomolecules.

Evaluation of Lipids and Lipid-Related Transcripts in Human and Ovine Theca Cells and an in Vitro Mouse Model Exposed to the Obesogen Chemical Tributyltin.

Exposure to obesogenic chemicals has been reported to result in enhanced adipogenesis, higher adipose tissue accumulation, and reduced ovarian hormonal synthesis and follicular function. We have reported that organotins [tributyltin (TBT) and triphenyltin (TPT)] dysregulate cholesterol trafficking in ovarian theca cells, but, whether organotins also exert lipogenic effects on ovarian cells remains unexplored. We investigated if environmentally relevant exposures to organotins [TBT, TPT, or dibutyltin (DBT)] induce lipid dysregulation in ovarian theca cells and the role of the liver X receptor (LXR) in this effect. We also tested the effect of TBT on oocyte maturation and neutral lipid accumulation, and lipid-related transcript expression in cumulus cells and preimplantation embryos. Primary theca cell cultures derived from human and ovine ovaries were exposed to TBT, TPT, or DBT (1, 10, or ). The effect of these chemical exposures on neutral lipid accumulation, lipid abundance and composition, lipid homeostasis-related gene expression, and cytokine secretion was evaluated using liquid chromatography-mass spectrometry (LC-MS), inhibitor-based methods, cytokine secretion, and lipid ontology analyses. We also exposed murine cumulus-oocyte complexes to TBT and evaluated oocyte maturation, embryo development, and lipid homeostasis-related mRNA expression in cumulus cells and blastocysts. Exposure to TBT resulted in higher intracellular neutral lipids in human and ovine primary theca cells. In ovine theca cells, this effect was dose-dependent, independent of cell stage, and partially mediated by LXR. DBT and TPT resulted in higher intracellular neutral lipids but to a lesser extent in comparison with TBT. More than 140 lipids and 9 cytokines were dysregulated in TBT-exposed human theca cells. Expression of genes involved in lipogenesis and fatty acid synthesis were higher in theca cells, as well as in cumulus cells and blastocysts exposed to TBT. However, TBT did not impact the rates of oocyte maturation or blastocyst development. TBT induced dyslipidemia in primary human and ovine theca cells, which may be responsible for some of the TBT-induced fertility dysregulations reported in rodent models of TBT exposure. https://doi.org/10.1289/EHP13955.

The Influence of Triphenyltin Exposure on the Osmoregulatory Capacity of Marine Medaka (Oryzias melastigma) at Different Salinities

Triphenyltin (TPT) is an organotin pollutant widely found in the aquatic environment. It has endocrine-disrupting and osmotic pressure toxicity. In this study, the physiological and biochemical effects of TPT and various salinities were investigated in different tissues (gut, gill, and brain) of marine medaka. The exposure experiments were conducted for 42 days in different salinities (0, 15, and 30 ppt) without TPT exposure and in different salinity groups with TPT exposure concentrations of 100 ng/L, respectively. The results showed that the Na+-K+-ATPase (NKA) and Ca2+ATPase activity had significant tissue-specific differences, with the highest activity observed in the gills, indicating their major contribution to osmoregulation. Changes in salinity also resulted in significant alterations in the ion concentrations of the gut and gill tissues in the 0-C and 15-C groups. While the changes in Na+ and Cl− were relatively stable, the presence of TPT disrupted the regulation of Ca2+ and K+. In conclusion, substantial variations were observed in the osmoregulatory capacity of marine medaka tissues. Environmental concentrations of TPT had little effect on osmotic enzyme activity but interfered with the regulation of Ca2+ and K+ concentrations in the tissues. This study provides valuable insights into the osmotic toxicity of TPT in aquatic environments with different salinities.

Triphenyltin induced darker body coloration by disrupting melanocortin system and pteridine metabolic pathway in a reef fish, Amphiprion ocellaris

Triphenyltin (TPT) is a typical persistent organic pollutant whose occurrence in coral reef ecosystems may threaten the survival of reef fishes. In this study, a brightly colored representative reef fish, Amphiprion ocellaris was used to explore the effects of TPT at environmental levels (1, 10, and 100 ng/L) on skin pigment synthesis. After the fish were exposed to TPT for 60 days, the skin became darker, owing to an increase in the relative area of black stripes, a decrease in orange color values while an increase in brown color values, and an increase in the number of melanocytes in the orange part of the skin tissues. To explore the mechanisms by which TPT induces darker body coloration, the enzymatic activity and gene expression levels of the members of melanocortin system that affect melanin synthesis were evaluated. Leptin levels and lepr expression were found to be increased after TPT exposure, which likely contributed to the increase found in pomc expression and α-melanocyte-stimulating hormone (α-MSH) levels. Then Tyr activity and mc1r, tyr, tyrp1, mitf, and dct were upregulated, ultimately increasing melanin levels. Importantly, RT-qPCR results were consistent with the transcriptome analysis of trends in lepr and pomc expression. Because the orange color values decreased, pterin levels and the pteridine metabolic pathway were also evaluated. The results showed that TPT induced BH4 levels and spr, xdh, and gch1 expression associated with pteridine synthesis decreased, ultimately decreasing the colored pterin content (sepiapterin). We conclude that TPT exposure interferes with the melanocortin system and pteridine metabolic pathway to increase melanin and decrease colored pterin levels, leading to darker body coloration in A. ocellaris. Given the importance of body coloration for the survival and reproduction of reef fishes, studies on the effects of pollutants (others alongside TPT) on body coloration are of high priority.

Transcriptomics-based analysis reveals the nephrotoxic effects of triphenyltin (TPT) on SD rats by affecting RAS, AQPs and lipid metabolism

Triphenyltin (TPT) is a class of organotin compounds that are extensively used in industry and agriculture. They have endocrine-disrupting effects and cause severe environmental contamination. Pollutants may accumulate in the kidneys and cause pathological complications. However, the mechanism of TPT's toxicological effects on the kidney remains unclear. This study aimed to investigate the toxic effects and mechanism of action of TPT exposure on renal impairment in rats. Male SD rats were divided into four groups: the Ctrl group (control group), TPT-L group (0.5 mg/kg/d), TPT-M group (1 mg/kg/d), and TPT-H group (2 mg/kg/d). After 28 days of exposure to TPT, we observed the morphology and structure of kidney tissue using HE, PASM, and Masson staining. We also detected serum biochemical indexes, performed transcriptome sequencing of rat kidney tissue using RNA-seq. Furthermore, protein expression levels were measured through immunohistochemistry and gene expression levels were determined using RT-qPCR. The study results indicated a decrease in kidney weight and relative kidney weight after 28 days of exposure to TPT. Additionally, TPT caused damage to kidney structure and function, as evidenced by HE staining, PASM staining, and serum biochemical tests. Transcriptomics identified 352 DEGs, and enrichment analyses revealed that TPT exposure primarily impacted the renin-angiotensin system (RAS). The expression levels of water channel proteins were reduced, and the expression levels of RAS and lipid metabolism-related genes (Mme, Ace, Fasn, Cyp4a8, Cpt1b and Ppard) were significantly decreased in the TPT-treated group. In summary, exposure to TPT may impair renal structure and function in rats by affecting RAS, AQPs, and lipid metabolism.

Novel triphenyltin(IV) compounds with carboxylato N-functionalized 2-quinolones as promising potential anticancer drug candidates: in vitro and in vivo evaluation.

Three newly synthesized triphenyltin(IV) compounds, Ph3SnL1 (L1- = 3-(4-methyl-2-oxoquinolin-1(2H)-yl)propanoato), Ph3SnL2 (L2- = 2-(4-methyl-2-oxoquinolin-1(2H)-yl)ethanoato), and Ph3SnL3 (L3- = 2-(4-hydroxy-2-oxoquinolin-1(2H)-yl)ethanoato), were characterized by elemental microanalysis, FT-IR spectroscopy and multinuclear (1H, 13C and 119Sn) NMR spectroscopy. A single X-ray diffraction study indicates that compounds Ph3SnL1 and Ph3SnL2 exhibit a 1D zig-zag chain polymeric structure, which in the case of Ph3SnL2 is additionally stabilized by π-interactions. In addition, the synthesized compounds were further examined using density functional theory and natural bond orbital analysis. The compounds have been evaluated for their in vitro anticancer activity against three human cell lines: MCF-7 (breast adenocarcinoma), A375 (melanoma), HCT116 (colorectal carcinoma), and three murine cell lines: 4T1 (breast carcinoma), B16 (melanoma), CT26 (colon carcinoma) using MTT and CV assays. The IC50 values fall in the nanomolar range, indicating that these compounds possess better anticancer activity than cisplatin. The study of the effect of the newly developed drug Ph3SnL1 showed its plasticity in achieving an antitumor effect in vitro, which depends on the specificity of the phenotype and the redox status of the malignant cell line and ranges from the initiation of apoptotic cell death to the induction of differentiation to a more mature cell form. In the syngeneic model of murine melanoma, Ph3SnL1 showed the potential to reduce the tumor volume similar to cisplatin, but in a well-tolerated form and with low systemic toxicity, representing a significant advantage over the conventional drug.

Triphenyltin Influenced Carotenoid-Based Coloration in Coral Reef Fish, Amphiprion ocellaris, by Disrupting Carotenoid Metabolism.

Triphenyltin (TPT), a kind of persistent pollutant, is prevalent in the aquatic environment and could pose a threat to coral reef fish. However, little is known about the toxicity of TPT on coral reef fish, especially regarding the representative characteristics of body coloration. Therefore, this study chose the clownfish (Amphiprion ocellaris) in order to investigate the effects of TPT exposure on its carotenoid-based body coloration under the environmentally relevant concentrations (0, 1, 10 and 100 ng/L). After TPT exposure for 60 d, the carotenoid contents were decreased and histological damage in the liver was found, shown as nuclear pyknosis and shift, lipid deposition and fibrotic tissue hyperplasia. Liver transcriptomic analysis showed that TPT exposure interfered with oxidative phosphorylation and fatty acid metabolism pathways, which related to carotenoids uptake and metabolism. Furthermore, TPT exposure led to oxidative damage in the liver, which is responsible for the changes in the antioxidant capacity of enzymes, including GSH, MDA, POD, CAT and T-SOD. TPT exposure also affected the genes (Scarb1, CD36, Stard3 and Stard5) related to carotenoid absorption and transport, as well as the genes (GstP1 and Bco2) related to carotenoid deposition and decomposition. Taken together, our results demonstrate that TPT influenced carotenoid-based coloration in coral reef fish by disrupting carotenoid metabolism, which complements the ecotoxicological effects and toxic mechanisms of TPT and provides data for the body color biology of coral reef fishes.

TMT-based quantitative proteomics analysis of Sprague-Dawley rats liver reveals Triphenyltin induced liver damage and lipid metabolism disorders

Triphenyltin (TPT) is a widely used pesticide that has a negative impact on biological health and production efficiency. In addition, TPT poses a threat to human health through the food chain and environmental pollution. However, the exact mechanism of TPT toxicity remains unclear. In this study, we investigated the hepatotoxicity of TPT and its effects on lipid metabolism using male SD rats as an animal model. Our results from HE and serum biochemical analysis suggested that TPT could damage liver structure and function, resulting in disruption of lipid metabolism. We therefore proceeded to analyze the proteomic response of rat liver tissue after 28 days of treatment with 2 mg/kg/d TPT. Our study demonstrates that TPT has a variety of effects on liver protein expression in rats. Through bioinformatic analysis, we observed significant changes in proteins related to fatty acid oxidation and synthesis due to TPT exposure. Furthermore, western blot and RT-qPCR experiments confirmed that TPT can affect lipid metabolism through the PPAR pathway. These findings suggest that TPT exposure can lead to liver damage, lipid accumulation and metabolic disorders.

Micro(nano)plastics in marine medaka: Entry pathways and cardiotoxicity with triphenyltin

The simultaneous presence of micro(nano)plastics (MNPs) and pollutants represents a prevalent environmental challenge that necessitates understanding their combined impact on toxicity. This study examined the distribution of 5 μm (PS-MP5) and 50 nm (PS-NP50) polystyrene plastic particles during the early developmental stages of marine medaka (Oryzias melastigma) and assessed their combined toxicity with triphenyltin (TPT). Results showed that 2 mg/L PS-MP5 and PS-NP50 could adhere to the embryo surface. PS-NP50 can passively enter the larvae and accumulate predominantly in the intestine and head, while PS-MP5 cannot. Nonetheless, both types can be actively ingested by the larvae and distributed in the intestine. 2 mg/L PS-MNPs enhance the acute toxicity of TPT. Interestingly, high concentrations of PS-NP50 (20 mg/L) diminish the acute toxicity of TPT due to their sedimentation properties and interactions with TPT. 200 μg/L PS-MNPs and 200 ng/L TPT affect complement and coagulation cascade pathways and cardiac development of medaka larvae. PS-MNPs exacerbate TPT-induced cardiotoxicity, with PS-NP50 exhibiting stronger effects than PS-MP5, which may be related to the higher adsorption capacity of NPs to TPT and their ability to enter the embryos before hatching. This study elucidates the distribution of MNPs during the early developmental stages of marine medaka and their effects on TPT toxicity, offering a theoretical foundation for the ecological risk assessment of MNPs.

Factors affecting the accumulation of organotins by wild fish: A case study in the Three Gorges Reservoir, China.

Organotin compounds (OTs) accumulate in fish easily, however, research on their influencing factors is still limited. This study collected 25 species of fish with different diets, habitats, and age from the Three Gorges Reservoir (TGR), the largest deep-water river channel-type reservoir in China, and analyzed the accumulation characteristics of OTs in these fish. The results showed that tributyltin (TBT) and triphenyltin (TPhT) were the dominant OTs in fish from the TGR. The correlation between OTs concentration and age, body length, and body weight varied with fish species. The concentrations of TBT and TPhT in carnivorous fish (mean, 25.78 and 11.69 ng Sn/g dw, respectively) were higher than those in other diet fish (P<0.01), but there was no significant difference in fish at different habitat water layers (P>0.05). In addition, the degradation rates of TBT and TPhT in different fish species were all below 50%. In summary, the accumulation of TBT and TPhT in fish is mainly influenced by diet, and both TBT and TPhT were difficult to degrade in fish. These results reveal the pollution characteristics of OTs in fish from the TGR, and can improve our understanding of the factors influencing TBT and TPhT accumulation in freshwater fish.

Protective effects of sulforaphane on inflammation, oxidative stress and intestinal dysbacteriosis induced by triphenyltin in Cyprinus carpio haematopterus

The purpose of this experiment was to study the mitigation effect of sulforaphane (SFN) on fish toxicological damage caused by triphenyltin (TPT) pollution. A total of 320 healthy fish (56.9 ± 0.4g) were randomly placed into four groups, each with four duplicates. The control group was fed the basal diet, the TPT group was exposed to 10 ng/L TPT on the basis of the control group, the SFN group was fed a diet supplemented with 10 mg/kg SFN, the SFN + TPT group was exposed to 10 ng/L TPT on the basis of the SFN group. Each tank had 20 fish and the breeding lasted for 8 weeks. The present study found that the antioxidant enzyme activity in the TPT group was significantly lower than that of the control group (P < 0.05). In addition, compared with the control group, the mRNA expression of pro-inflammatory factors (IL-6, TNF-α) were significantly induced, and the anti-inflammatory factor genes (IL-10, TGF) were significantly inhibited (P < 0.05) in TPT group. SFN relieved the changes of inflammatory factors caused by TPT, ameliorated oxidative stress, improved antioxidant enzyme (include SOD, CAT, GSH, GPx) activities (P < 0.05). 16s RNA analysis indicated that exposure to TPT caused changes in intestinal microflora. The results of the study showed that after exposure to TPT, some beneficial genera of bacteria in the gut of Rhizobiaceae, Bdellovibrio and Candidatus Alysiosphaera were decreased. The bacteria associated with intestinal inflammation including Propionibacterium, Rubrobacter, Anaerorhabdus_furcosa_group, Rikenellaceae and Eubacterium_brachy were upregulated. However, the SFN treatment group significantly down-regulated the above five inflammation-related bacteria. The above results indicated that TPT caused oxidative stress and inflammation in fish intestines, changed the intestinal microflora, and dietary SFN could improve antioxidant status, regulate inflammation and intestinal health. Therefore, SFN is a promising diet additive for improving fish damage caused by TPT contamination.

Short-term triphenyltin exposure alters microbial homeostasis in the silkworm (Bombyx mori) midgut

Triphenyltin (TPT) is a widespread synthetic chemical used in many fields and its potential risk to organisms has been comprehensively investigated using different animal models and species. Currently, little is known about the effects of TPT exposure on microbial midgut diversity, therefore we explored these effects in the lepidopterous silkworm model using 16S rDNA sequencing. In total, 5273 and 5065 operational taxonomic units (OTUs) were identified in control and TPT-exposure group samples, ranging from 424 to 728 OTUs/sample. Alpha-diversity analyses revealed that TPT exposure induced the fluctuations of gut microbial diversity and abundance while beta-diversity analyses identified a distinct impact on major gut microbiota components. In our microbiome analyses, 23 phyla and 353 genera were recognized in the control group, while 20 phyla and 358 genera were recognized in the TPT exposure group. At the genus level, midgut microbiota were composed of several predominant bacterial genera, including Muribaculaceae, Lactobacillus, and UCG-010. In the TPT exposure group, o__Bacillales, f__Bacillaceae, and f__Caldicoprobacteraceae abundance was relatively high, while f__Oscillospiraceae, f__Fusobacteriaceae, and f__SC_I_84 abundance was relatively high in the control group. Gene function analyses in silkworm microbiota after TPT exposure showed that biosynthesis of ansamycins, fructose and mannose metabolism, glycerolipid metabolism, type II diabetes mellitus, glycolysis/gluconeogenesis, lipid metabolism, translation proteins, atrazine degradation, DNA repair and recombination proteins, nicotinate and nicotinamide metabolism were significantly increased. Collectively, our silkworm model identified gut microbial diversity risks and the adverse effects from TPT exposure, which were similar to other aquatic animals. Therefore, TPT levels in environmental samples must be monitored to prevent ecological harm.

4-Aminoantipyrine-new organotin complexes, synthesis, structure and antioxidant activity

ABSTRACT. 4-Aminoantipyrine was used as ligand to prepare new complexes of triphenyltin, di-butyl and dimethyl-tin complexes by condensation reaction with the corresponding organotin chloride salts. The complexes were identified by different techniques, such as infrared spectra, (tin and proton) magnetic resonance and elemental analyses. The antioxidant activity of 4-aminoantipyrine and prepared complexes were studied by two different methods; Free radical scavenging activity DPPH and CUPRRAC methods. Tri and di-tin complexes gave high percentage inhibition than ligand with both methods due to tin moiety, also triphenyltin carboxylate complex was the best compared with the others.&#x0D; &#x0D; KEY WORDS: 4-Aminoantipyrine, Condensation, Triphenyl tin chloride, DPPH and CUPRRAC methods&#x0D; Bull. Chem. Soc. Ethiop. 2023, 37(5), 1163-1170. &#x0D; DOI: https://dx.doi.org/10.4314/bcse.v37i5.9