Tributyltin Research Articles

Tributyltin Enhances Macrophage Inflammation and Lipolysis, Contributing to Adipose Tissue Dysfunction.

Tributyltin (TBT) is a synthetic chemical widely used in industrial and commercial applications. TBT exposure has been proven to elicit obesogenic effects. Gestational exposure led to increased white adipose tissue depot size in exposed (F1, F2) animals and in unexposed generations (F3, F4), an example of transgenerational inheritance. TBT exerts these effects in part by increasing the number and size of white adipocytes, altering the fate of multipotent mesenchymal stromal stem cells to favor the adipocyte lineage, altering adipokine secretion, and modulating chromatin structure. Adipose tissue resident macrophages are critical regulators in adipose tissue; however, the effects of TBT on adipose tissue macrophages remained unclear. Here we investigated the effects of TBT on macrophages and consequent impacts on adipocyte function. TBT significantly enhanced palmitate-induced inflammatory gene expression in mouse bone marrow derived macrophages and this effect was attenuated by the antagonizing action of the nuclear receptor peroxisome proliferator activated receptor gamma. TBT-treated macrophages decreased lipid accumulation in white adipocytes differentiated from mesenchymal stromal stem cells accompanied by increased expression of lipolysis genes. Lastly, ancestral TBT exposure increased Tnf expression in adipose tissue resident macrophages in both exposed (F2) and unexposed (F3) generations, suggesting that TBT exposure led to an inherited predisposition toward inflammatory adipose tissue macrophages that can manipulate adipose tissue function. These findings provide new insights into the interplay between adipocytes and adipose tissue macrophages in obesity, further establishing a role for obesogens such as TBT in the development of obesity-related metabolic disorders.

Endocrine-Disrupting Chemicals, Hypothalamic Inflammation and Reproductive Outcomes: A Review of the Literature.

Endocrine-disrupting chemicals (EDCs) are environmental and industrial agents that interfere with hormonal functions. EDC exposure is linked to various endocrine diseases, especially in reproduction, although the mechanisms remain unclear and effects vary among individuals. Neuroinflammation, particularly hypothalamic inflammation, is an emerging research area with implications for endocrine-related diseases like obesity. The hypothalamus plays a crucial role in regulating reproduction, and its inflammation can adversely affect reproductive health. EDCs can cross the blood-brain barrier, potentially causing hypothalamic inflammation and disrupting the reproductive axis. This review examines the existing literature on EDC-mediated hypothalamic inflammation. Our findings suggest that exposure to 2,3,7,8-tetrachloro-dibenzo-p-dioxin (TCDD), polychlorinated biphenyl (PCB), tributyltin (TBT), phthalates, bisphenol A (BPA), and chlorpyrifos (CPF) in animals is linked to hypothalamic inflammation, specifically affecting the hypothalamic centers of the gonadotropic axis. To our knowledge, this is the first comprehensive review on this topic, indicating hypothalamic inflammation as a possible mediator between EDC exposure and reproductive dysfunction. Further human studies are needed to develop effective prevention and treatment strategies against EDC exposure.

Investigating tributyltin's toxic effects: Intestinal barrier and neuroenteric disruption in rat’s jejunum

The expansion of economic activities in coastal areas has significantly increased chemical contamination, leading to major environmental challenges. Contaminants enter the human body through the food chain, particularly via seafood and water consumption, triggering biomagnification and bioaccumulation processes. The gastrointestinal tract (GIT) acts as a selective barrier, protecting against chemical pollutants and maintaining homeostasis through a complex network of cells and immune responses. This study assessed impact of tributyltin (TBT), a highly toxic organometallic compound used in antifouling coatings for ships, on the GIT and myenteric neural plasticity in young rats. TBT exposure leads to histopathological changes, including epithelial detachment and inflammatory foci, especially at lower environmental doses. The study found that TBT causes significant reductions in villi height, increases in goblet cells and intraepithelial lymphocytes, and disrupts the myenteric plexus, with higher densities of extraganglionic neurons in exposed animals.

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.

Development of methodology for the visual identification of Tributyltin (TBT) in antifouling paint matrices.

Organotin compounds (OTC), mainly tributyltin (TBT), have been used since the 1970s as biocides in the composition of antifouling paints. Due to its physical-chemical characteristics, TBT has high toxicity to the marine environment affecting non-target organisms. The present study aims to develop a method of direct visual identification of TBT in antifouling paints using the cyclopalladate complex, 4- (2-thiazolylazo) resorcinol (TAR-Pd), synthesized in our laboratory. Tests were performed in blank and in the paint matrix with the following OTC: TBT-O; TBT-Cl; TPT-Cl; DBT-Cl (tributyltin oxide, tributyltin chloride, triphenyltin chloride, dibutyltin chloride), in addition to the SnCl4 and SnCl2 compounds (tin IV chloride and tin II chloride), all at a concentration of approximately 20g/ kg of dry paint). The test was performed by applying paint samples to test bodies and scraping a few tens of milligrams of the dry paint film. The scraped paint samples were submitted to the test, showing a different staining reaction for the TBT-Cl and SnCl4 samples concerning blank and other samples (TBT-O, TPT, DBT-Cl, and SnCl2). Solution tests were performed to characterize reaction products by spectroscopy in the visible band. The method developed has potential for application in real samples, being selective for TBT-Cl and SnCl4 in an acid medium, obtaining a limit of detection, in the range of 1-10mg/kg dry paint.

In Vivo Evaluation of The Hepatotoxic Disorders of Tributyltin Low Doses in Male Rats

Tributyltin (TBT) has been used widely for over 60 years as a pesticidal, preservation, rodent repellent, water-repellant coating, corrosion inhibitor, flame-resistant polyester, and household product. Previous research has demonstrated the toxicity of high doses of TBT, but there is insufficient data on the effects of relevant levels of TBT on at low doses. The main goal of this thesis is to recognize the hepatotoxicity of Sublethal doses of TBT chloride (10-2000 µg/Kg body weight) in male rats for 45 days. TBT induced hepatic induction of oxidative stress as indicated by increasing levels of TBARS and 8-OHdG, induction of hepatic inflammation as indicated by the elevated NF-B levels; inhibition of hepatic expression of PGC-1α and impairment of mitochondrial biogenesis, induction of SREBP-1c and induce hepatic lipogenesis and fatty liver, and distortion of hepatic structure at histological level in a dose-dependent manner significantly at doses higher than 250 µg/kg. In conclusion: the TBT at low doses can induce hepatotoxicity at different levels.

Spatial and temporal distribution of tributyltin in the coastal environment of the Croatian Adriatic (2016-2023): TBT remains a cause for concern

This work presents a spatial and temporal distribution of tributyltin (TBT) and TBT pollution assessment of the Croatian Adriatic coast in the period 2016 – 2023. The monitoring of TBT pollution was carried out within the Water Framework Directive (2000/60/EC) and the Marine Strategy Framework Directive (2008/56/EC). TBT concentrations were measured at 63 sites in coastal and transitional waters in three compartments - water, sediments and mussels. The ranges of TBT concentrations were <0.06 – 6.40 ng(TBT)/L in the water column, <1 – 2546 ng(TBT)/g(d.w.) in sediments, and <1 – 655 ng(TBT)/g(d.w.) in mussels, while transitional waters were in general more polluted than coastal waters. Monitoring of TBT concentrations in water showed that 30% of monitored sites were continuously polluted with TBT with average annual concentrations exceeding AA-EQS [0.2 ng(TBT)/L], while 20% of the sites had concentrations in sediments above the proposed EQS for sediments [1.6 ng(TBT)/g(d.w.)]. In mussels, TBT was detected at 70% of the sites with more than 60% of the sites exceeding the OSPAR criteria [12.6 ng(TBT)/g(d.w.)], indicating that the occurrence of imposex in gastropods at these sites is very likely. Only a slight decrease in TBT levels was observed over the investigated period, but concentrations at most contaminated sites did not fall below the EQS. This study shows that, despite the ban of TBT-based antifouling paints more than 15 years ago (except for public and military vessels), contamination of the Croatian Adriatic coast with TBT still exists and regular monitoring is essential. The TBT distribution was primarily determined by the vicinity of the pollution source, i.e. shipping traffic, but the role of physicochemical parameters, such as dissolved organic carbon (DOC) and transparency of the water column, should not be disregarded as well as the influence of hydrodynamics in the transitional waters. Although monitoring of TBT concentrations in water is an established approach to assess recent pollution, this long-term study has shown that mussels can be the most reliable indicator of pollution in a given area over the last several months.

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.

A Chemical Toolbox to Unveil Synthetic Nature-Inspired Antifouling (NIAF) Compounds.

The current scenario of antifouling (AF) strategies to prevent the natural process of marine biofouling is based in the use of antifouling paints containing different active ingredients, believed to be harmful to the marine environment. Compounds called booster biocides are being used with copper as an alternative to the traditionally used tributyltin (TBT); however, some of them were recently found to accumulate in coastal waters at levels that are deleterious for marine organisms. More ecological alternatives were pursued, some of them based on the marine organism mechanisms' production of specialized metabolites with AF activity. However, despite the investment in research on AF natural products and their synthetic analogues, many studies showed that natural AF alternatives do not perform as well as the traditional metal-based ones. In the search for AF agents with better performance and to understand which molecular motifs were responsible for the AF activity of natural compounds, synthetic analogues were produced and investigated for structure-AF activity relationship studies. This review is a comprehensive compilation of AF compounds synthesized in the last two decades with highlights on the data concerning their structure-activity relationship, providing a chemical toolbox for researchers to develop efficient nature-inspired AF agents.

Tributyltin-induced visceral adiposity is associated with impaired redox balance in white adipose tissue of male rats

Tributyltin (TBT) is an organotin compound that has several adverse health effects, including the development of obesity. Although obesity is strongly associated with adipose redox imbalance, there is a lack of information on whether TBT promotes a pro-oxidative environment in WAT. Thus, adult male Wistar rats were randomly exposed to either vehicle (ethanol 0.4%) or TBT (1000 ng/kg) for 30 days. Body and fat pad masses, visceral fat morphology, lipid peroxidation, protein carbonylation, redox status markers, and catalase activity were evaluated. TBT promoted increased adiposity and visceral fat, with hypertrophic adipocytes, but did not alter body mass and subcutaneous fat. ROS production and lipid peroxidation were elevated in TBT group, as well as catalase protein expression and activity, although protein oxidation and glutathione peroxidase protein expression remained unchanged. In conclusion, this is the first study to demonstrate that subacute TBT administration leads to visceral adipose redox imbalance, with increased oxidative stress. This enlights the understanding of the metabolic toxic outcomes of continuous exposure to TBT in mammals.

Tributyltin induces apoptosis in mammalian cells invivo: a scoping review.

The present review aimed to evaluate the apoptotic effect of tributyltin (TBT) exposure on mammalian tissues and cells invivo. A search was conducted in specialized literature databases including Embase, Medline, Pubmed, Scholar Google, and Scopus for all manuscripts using the following keywords: "tributyltin", "apoptosis", "mammals", "mammalian cells', "eukaryotic cells", 'rodents', "rats", "mice" and "invivo" for all data published until September 2023. A total of 16 studies were included. The studies have demonstrated that TBT exposure induces apoptosis in cells from various mammalian organs or tissues invivo. TBT is capable to increase apoptotic cells, to activate proapoptotic proteins such as calpain, caspases, bax andbeclin-1 and to inhibit antiapoptotic protein bcl-2. Additionally, TBT alters the ratio of bcl-2/bax which favor apoptosis. Therefore, the activation of enzymes such as calpain induces apoptosis mediated by ERS and caspases through the intrinsic apoptosis pathway. This review has demonstrated that TBT exposure induces apoptosis in mammalian tissues and cells invivo.

Effect of tributyltin exposure on the embryonic development and behavior of a molluscan model species, Lymnaea stagnalis

The presence of the organotin compound tributyltin (TBT) in aquatic ecosystems has been a serious environmental problem for decades. Although a number of studies described the negative impact of TBT on mollusks at different levels, investigations connected to its potential effects during embryogenesis have been neglected. For a better understanding of the impact of TBT on mollusks, in the present study, embryos of previously TBT-treated or not treated specimens of the great pond snail (Lymnaea stagnalis) were exposed to 100 ng L−1 TBT from egg-laying (single-cell stage) until hatching. According to our results, TBT significantly delayed hatching and caused shell malformation. TBT transiently decreased the locomotion (gliding) and also reduced the feeding activity, demonstrating for the first time that this compound can alter the behavioral patterns of molluscan embryos. The heart rate was also significantly reduced, providing further support that cardiac activity is an excellent indicator of metal pollution in molluscan species. At the histochemical level, tin was demonstrated for the first time in TBT-treated hatchlings with intensive reaction in the central nervous system, kidney, and hepatopancreas. Overall, the most notable effects were observed in treated embryos derived from TBT treated snails. Our findings indicate that TBT has detrimental effects on the development and physiological functions of Lymnaea embryos even at a sub-lethal concentration, potentially influencing their survival and fitness. Highlighting our observations, we have demonstrated previously unknown physiological changes (altered heart rate, locomotion, and feeding activity) caused by TBT, as well as visualized tin at the histochemical level in a molluscan species for the first time following TBT exposure. Further studies are in progress to reveal the cellular and molecular mechanisms underlying the physiological and behavioral changes described in the present study.

Endocrine disruption of adipose physiology: Screening in SGBS cells.

The increasing use of industrial chemicals has raised concerns regarding exposure to endocrine-disrupting chemicals (EDCs), which interfere with developmental, reproductive and metabolic processes. Of particular concern is their interaction with adipose tissue, a vital component of the endocrine system regulating metabolic and hormonal functions. The SGBS (Simpson Golabi Behmel Syndrome) cell line, a well-established human-relevant model for adipocyte research, closely mimics native adipocytes' properties. It responds to hormonal stimuli, undergoes adipogenesis and has been successfully used to study the impact of EDCs on adipose biology. In this study, we screened human exposure-relevant doses of various EDCs on the SGBS cell line to investigate their effects on viability, lipid accumulation and adipogenesis-related protein expression. Submicromolar doses were generally well tolerated; however, at higher doses, EDCs compromised cell viability, with cadmium chloride (CdCl2) showing the most pronounced effects. Intracellular lipid levels remained unaffected by EDCs, except for tributyltin (TBT), used as a positive control, which induced a significant increase. Analysis of adipogenesis-related protein expression revealed several effects, including downregulation of fatty acid-binding protein 4 (FABP4) by dibutyl phthalate, upregulation by CdCl2 and downregulation of perilipin 1 and FABP4 by perfluorooctanoic acid. Additionally, TBT induced dose-dependent upregulation of C/EBPα, perilipin 1 and FABP4 protein expression. These findings underscore the importance of employing appropriate models to study EDC-adipocyte interactions. Conclusions from this research could guide strategies to reduce the negative impacts of EDC exposure on adipose tissue.

Subacute exposure to a mixture of tributyltin plus mercury impairs reproductive axis function, exacerbating premature ovarian insufficiency features and reducing fertility in female rats

Tributyltin (TBT) and mercury (Hg) are endocrine-disrupting chemicals that individually cause reproductive complications. However, the reproductive consequences of exposure to a mixture of TBT plus Hg are not well known. We hypothesized that exposure to a mixture of TBT plus Hg would alter hypothalamic-pituitary-gonadal (HPG) axis function. Female rats were exposed to this mixture daily for 15 days, after which chemical accumulation in the tissues, morphology, hormone levels, inflammation, fibrosis, and protein expression in the reproductive organs were assessed. Increases in tin (Sn) and Hg levels were detected in the serum, HPG axis, and uterus of TBT-Hg rats. TBT-Hg rats exhibited irregular estrous cycles. TBT-Hg rats showed an increase in gonadotropin-releasing hormone (GnRH) protein expression and follicle-stimulating hormone (FSH) levels and a reduction in luteinizing hormone (LH) levels. Reduced ovarian reserve, antral follicles, corpora lutea (CL) number, and estrogen levels and increased atretic and cystic follicles were found, suggesting that TBT-Hg exposure exacerbated premature ovarian insufficiency (POI) features. Furthermore, TBT-Hg rats exhibited increased ovarian mast cell numbers, expression of the inflammatory markers IL-6 and collagen deposition. Apoptosis and reduced gland number were observed in the uteri of TBT-Hg rats. A reduction in the number of pups/litter for 90 days was found in TBT-Hg rats, suggesting impaired fertility. Strong negative correlations were found between serum and ovarian Sn levels and ovarian Hg levels and ovarian reserve and CL number. Collectively, these data suggest that TBT plus Hg exposure leads to abnormalities in the HPG axis, exacerbating POI features and reducing fertility in female rats.

Subacute tributyltin exposure alters the development and morphology of mammary glands in association with CYP19A1 expression in female rats

Tributyltin (TBT) is an endocrine-disrupting chemical (EDC) related to reproductive dysfunctions. However, few studies have investigated the effects of TBT exposure on mammary gland development. Thus, we assessed whether subacute TBT exposure causes irregularities in mammary gland development. We administered TBT (100 and 1,000 ng/kg/day for 30 days) to female rats from postnatal day (PND) 25 to PND 55, and mammary gland development, morphology, inflammation, collagen deposition, and protein expression were evaluated. Abnormal mammary gland development was observed in both TBT groups. Specifically, TBT exposure reduced the number of terminal end buds (TEBs), type 1 (AB1) alveolar buds, and type 2 (AB2) alveolar buds. An increase in the lobule and differentiation (DF) 2 score was found in the mammary glands of TBT rats. TBT exposure increased mammary gland blood vessels, mast cell numbers, and collagen deposition. Additionally, both TBT rats exhibited intraductal hyperplasia and TEB-like structures. An increase in estrogen receptor alpha (ERα), progesterone receptor (PR), and cytochrome P450 family 19 subfamily A member 1 (CYP19A1) - positive cells was observed in the mammary glands of TBT rats. A strong negative correlation was observed between CYP19A1- positive cells and TEB number. In addition, CYP19A1 - positive cells were positively correlated with mammary gland TEB-like structure, ductal hyperplasia, inflammation, and collagen deposition. Thus, these data suggest that TBT exposure impairs mammary gland development through the modulation of CYP19A1 signaling pathways in female rats.

Synergistic Steatosis Induction in Mice: Exploring the Interactions and Underlying Mechanisms between PFOA and Tributyltin.

This study explores the impact of environmental pollutants on nuclear receptors (CAR, PXR, PPARα, PPARγ, FXR, and LXR) and their heterodimerization partner, the Retinoid X Receptor (RXR). Such interaction may contribute to the onset of non-alcoholic fatty liver disease (NAFLD), which is initially characterized by steatosis and potentially progresses to steatohepatitis and fibrosis. Epidemiological studies have linked NAFLD occurrence to the exposure to environmental contaminants like PFAS. This study aims to assess the simultaneous activation of nuclear receptors via perfluorooctanoic acid (PFOA) and RXR coactivation via Tributyltin (TBT), examining their combined effects on steatogenic mechanisms. Mice were exposed to PFOA (10 mg/kg/day), TBT (5 mg/kg/day) or a combination of them for three days. Mechanisms underlying hepatic steatosis were explored by measuring nuclear receptor target gene and lipid metabolism key gene expressions, by quantifying plasma lipids and hepatic damage markers. This study elucidated the involvement of the Liver X Receptor (LXR) in the combined effect on steatosis and highlighted the permissive nature of the LXR/RXR heterodimer. Antagonistic effects of TBT on the PFOA-induced activation of the Pregnane X Receptor (PXR) and Peroxisome Proliferator-Activated Receptor Gamma (PPARγ) were also observed. Overall, this study revealed complex interactions between PFOA and TBT, shedding light on their combined impact on liver health.

Environmental matrices effect in butyltin determinations by GC/MS

The present study evaluated the matrix effect associated to determination of butyltin compounds (tripropyltin (TPrT), tributyltin (TBT), dibutyltin (DBT) and monobutyltin (MBT)) in sediment and mussel tissues using derivatization by Grignard reaction and quantification by gas chromatography coupled mass spectrometry (GC-MS). A non-negligible matrix effect was verified for sediments (54.2, 20.3, 13.6 and -53.6 %) and mussel tissues (-12.5, -32.0, 59.4 and 65.7 %) for TPrT, TBT, DBT and MBT respectively. However, this matrix effect was prevailed by preparing the analytical curves using standard addition techniques. Thus, an analytical method was optimized and validated for a more accurate and precise determination of butyltin compounds in sediment and mussel tissue samples.

Long-term tributyltin exposure alters behavior, oocyte maturation, and histomorphology of the ovary due to oxidative stress in adult zebrafish

Tributyltin (TBT), an organotin endocrine-disrupting substance, is recognized as one of the important toxic environmental pollutants. The present study was carried out to investigate the toxic effects of TBT on behavior and the ovary of adult zebrafish with a focus on oxidative stress markers and oocyte maturation. Adult zebrafish were exposed to three different concentrations (125, 250, and 500 ng/L of water) of TBT for 28 days. TBT exposure produced a concentration-dependent negative effect on the body weight and behavior (anxiety-like symptoms) of adult zebrafish. Alterations in the activity of superoxide dismutase (SOD) and catalase (CAT), the total antioxidant capacity of ovarian tissue by the highest exposure level of TBT resulted in lipid peroxidation as indicated by increased malondialdehyde (MDA) level. The numbers of early-vitellogenic oocytes were significantly increased in zebrafish exposed to TBT as low as 125 ng/L. However, the numbers and size of fully-grown (mature) oocytes were significantly reduced in the highest exposure group only. Correlation between the MDA level and pre-vitellogenic oocytes in the 500 ng/L group indicated that lipid peroxidation prevented the maturation of pre-vitellogenic oocytes. TBT exposure produced significant histological changes in the ovary as evidenced by disturbed maturation of oocytes. In conclusion, TBT adversely affected the maturation of oocytes in zebrafish ovary through oxidative stress-mediated mechanisms.

Microcosm study reveals the microbial and environmental effects on tributyltin degradation in an estuarine sediment

Tributyltin (TBT) is one of the most harmful contaminants ever released into the aquatic environment. Despite being banned, it is still present at many locations throughout the world. Its degradation in sediment mainly occurs through microbial biodegradation, a process that remains unclear. This study therefore aimed at better understanding TBT biodegradation in estuarine sediment and the microbial community associated with it. Microcosm experiments were set up, embracing a range of environmental control parameters. Major community shifts were recorded, mainly attributed to the change in oxygen status. The highest percentage of degradation (36,8%) occurred at 4 °C in anaerobic conditions. These results are encouraging for the in-situ bioremediation of TBT contaminated muddy sediment in temperate ports worldwide. However, with TBT able to persist in the coastal environment for decades when undisturbed in anoxic sediment, further research is needed to fully understand the mechanisms that triggered this biodegradation observed in the microcosms.

Tributyltin (TBT) toxicity: Effects on enteric neuronal plasticity and intestinal barrier of rats' duodenum

Tributyltin (TBT) is a biocide used in the formulation of antifouling paints and it is highly harmful. Despite the ban, the compound persists in the environment, contaminating marine foodstuffs and household products. Therefore, considering the route of exposure to the contaminant, the gastrointestinal tract (GIT) acts as an important barrier against harmful substances and is a potential biomarker for understanding the consequences of these agents. This work aimed to evaluate histological and neuronal alterations in the duodenum of male Wistar rats that received 20 ng/g TBT and 600 ng/g via gavage for 30 consecutive days. After the experimental period, the animals were euthanized, and the duodenum was intended for neuronal histochemistry (total and metabolically active populations) and histological routine (morphometry and histopathology). The results showed more severe changes in neuronal density and intestinal morphometry in rats exposed to 20 ng/g, such as total neuronal density decrease and reduction of intestinal layers. In rats exposed to 600 ng/g of TBT, it was possible to observe only an increase in intraepithelial lymphocytes. We conclude that TBT can be more harmful to intestinal homeostasis when consumed in lower concentrations.