Microplastics (MPs), emerging as significant pollutants, have been consistently detected in aquatic environments, with the Yangtze River experiencing a particularly severe level of microplastic pollution, exceeding all other watersheds in China. Polypropylene (PP), the plastic most abundantly found in the middle and lower reaches of the Yangtze River Basin, has less comprehensive research results into its toxic effects. Consequently, the present investigation employed zebrafish as a model organism to delve into the toxicological impacts of polypropylene microplastics (PP-MPs) with a diameter of 5 μm across varying concentrations (300 mg/L and 600 mg/L). Using histopathological, microbiota profiling, and transcriptomic approaches, we systematically evaluated the impact of PP-MPs exposure on the intestine and liver of zebrafish. Histopathological analysis revealed that exposure to PP-MPs resulted in thinner intestinal walls, damaged intestinal mucosa, and hepatic cellular damage. Intestinal microbiota profiling demonstrated that, the richness, uniformity, diversity, and homogeneity of gut microbes significantly increased after the PP-MPs exposure at high concentration. These alterations were accompanied by shifts in the relative abundance of microbiota associated with intestinal pathologies, suggesting a profound impact on the intestinal microbial community structure. Concurrently, hepatic transcriptome analysis and RT-qPCR indicated that the downregulation of pathways and genes associated with cell proliferation regulation and DNA damage repair mechanisms contributed to hepatic cellular damage, ultimately exerting adverse effects on the liver. Correlation analysis between the intestinal microbiota and liver transcriptome profiles further highlighted significant associations between intestinal microbiota and the downregulated hepatic pathways. Collectively, these results provide novel insights into the subacute toxicological mechanisms of PP-MPs in aquatic organisms and highlight the need for further research on the ecological and health risks associated with PP-MPs pollution.

The bio-reductive fabrication of nanomaterials is a developing arena of study that seeks to fabricate nanoparticles (NPs) using microorganisms, plants, and animal blood. However, the chemical approach of AgNPs fulfills the need of abundant need of NPs. In contrast, chemically fabricated AgNPs are more toxic than biological AgNPs. Therefore, the current study aimed to assess and evaluate the chemically fabricated silver nanoparticles (AgNPs) for their possible toxicity in Common carp fish (Cyprinus carpio). The chemically synthesized silver nanoparticles were purchased from the market and applied for their possible toxicity. The chemically fabricated AgNPs were used against the Cyprinus carpio for bioaccumulation in different organs and histological alterations in the intestine and muscles. The results revealed that the AgNPs were mostly accumulated in the intestines followed by the gills, liver, and muscles (p < .05). The accumulated AgNPs caused histological alterations in gills and intestines at the highest concentration (0.08 mg/L). However, no alterations were observed by the middle and lowest concentration of AgNPs, particularly, in the intestine. In conclusion, more extensive research is required to establish the hazards related to the use of nanoparticles to disclose their negative effects on fish and the aquatic environment. REASEARCH HIGHLIGHTS: The chemical method fabricates a large amount of AgNPs Additionally, considered more toxic than the bio-reductive method AgNPs have excellent and diverse applications AgNPs deposited in various organs and cause histological changes.

Silver nanoparticles (AgNPs) are widely used and have various applications, including medicine, electronics, and textiles. However, their increasing use raises concern about their potential environmental impact, particularly on aquatic organisms, such as fish, which are the primary consumers of aquatic environments and can be exposed to AgNPs through various routes. For this purpose, the leaves of the plant species Bellis perennis were used as a reductive agent to convert silver nitrate into AgNPs, to assess its toxicity against fish. Well-dispersed and undersized AgNPs were obtained and confirmed using analytical techniques, including Scanning Electron Microscopy (SEM) and Transmission Electron Microscopy (TEM). Moreover, the AgNPs have shown significant antibacterial activity against Aeromonas hydrophila (25.71 ± 0.63) and Vibrio harveyi (22.39 ± 0.29). In addition, the toxicity of the obtained AgNPs was assessed by exposing Cyprinus carpio to various concentrations, including 0.06, 0.1, and 0.2 mg/L. The findings revealed that the AgNPs were significantly accumulated in the intestine, followed by the gills, liver, muscles, kidney, and brain. This bioaccumulation led to histological alterations and destruction in the villi of the intestine, regeneration of liver cells, and degeneration of the gill lamella. RESEARCH HIGHLIGHTS: Plants based synthesis of AgNPs is mostly considered as eco-friendly A significant antibacterial activity was obtained The plant mediated AgNPs were found less toxic The AgNPs was profoundly accumulated and causes histological alterations.

Melamine is an important chemical raw material used in industries, which has potential health risks to animals and humans. Current research mainly focuses on the toxic effects of high-dose melamine ingestion. However, there are few reports on whether melamine at the current limited standard dose has adverse effects on various tissues and organs, and whether there are sensitive target genes for risk evaluation. For this, 24 female Kunming mice were fed 0, 1.8-, 3.6-, and 7.2- mg/kg/d melamine via drinking water for consecutive 28 days, respectively. The morphological changes of the ovarian, hepatic, and renal tissues were firstly observed. The results demonstrated that the histopathology of ovary, liver, and especially in kidney had been altered by melamine intake in female. And then, the transcriptional levels of MAPK signaling genes including p38, ERK1, ERK2, JNK1, and JNK2 in kidneys were investigated by real-time PCR. The data showed that ERK1 and p38 mRNAs expressions were up-regulated significantly by melamine, suggesting that ERK1 and p38 transcriptional levels in the kidney might to be considered as candidate targets for lower-dose melamine toxicity. This study not only provides potential targets for the diagnosis and prevention of melamine damage, but also helps to assess the health risks of the current minimum allowable levels of melamine in food and environment.

Antimicrobial additives in personal care products (PCPs) such as triclosan (TCS) and triclocarban (TCC) are of environmental concern due to their potential toxicity in non-target aquatic organisms. In this study, the histological, genotoxic (micronucleus assay), and embryotoxic effects of sublethal and environmentally relevant concentrations of TCS and TCC were evaluated in Clarias gariepinus (the African sharptooth catfish) over a period of 28 days. The 96 hLC50 values of TCS and TCC against fingerlings of C. gariepinus were 16.04 mg/L and 41.57 mg/L respectively. The 24 hLC50 and 26 hEC50 (non-hatching) values for C. gariepinus embryos were 16.48 mg/L and 11.08 mg/L for TCS and 46.08 mg/L and 41.93 mg/L for TCC respectively. TCS was ×3 to ×4 more toxic to C. gariepinus fingerlings and embryos than TCC. Gill histological alterations ranged from mild to severe lamellar necrosis in the exposed fishes with Gill Alteration Index (GAI) of 1.60 on day 14 and 3.20 on day 28. There were significant dose-dependent increases (p < 0.05) in micronuclei and binucleated cells in the erythrocytes of exposed fishes compared to control. Embryotoxic effects assessed from 0 to 72 h post fertilization showed significant decreases (p < 0.05) in hatching success and number of heartbeats per minute, and significant increase (p < 0.05) in percentage abnormalities in the exposed embryos compared to control. The study demonstrates the need for regulatory measures and monitoring of the use of TCS and TCC in PCPs in order to mitigate potential adverse effects to non-target aquatic organisms. This will support the United Nations Sustainable Development Goal 14 on sustaining life below water.

The increasing application and subsequent mass production of graphene-family materials (GFMs) will lead to greater possibilities for their release into the environment. Although GFMs exhibit toxicity toward various aquatic organisms, little information is available on their influence on gut microbiota of aquatic organism. In this study, zebrafish were fed diets containing three GFMs, namely, monolayer graphene powder (GR), graphene oxide nanosheet (GO) and reduced graphene oxide powder (rGO), or appropriate control for 21 days. The gut bacterial communities were then characterized for comparison of the exposure effects of each GFM. Alterations of the intestinal morphology and oxidative stress indicators were also examined. The results showed GFMs led to different inflammatory responses and significantly altered the relative composition of the gut bacterial species by increasing the relative abundance of Fusobacteria and the genus Cetobacterium and Lactobacillus and decreasing the abundance of Firmicutes and the genus Pseudomonas; GR caused marked shifts in the diversity of the gut microbiota. The GFMs also altered the intestinal morphology and antioxidant enzyme activities by inducing more vacuolation and generating more goblet cells. Our findings demonstrate that GFM exposure poses potential health risks to aquatic organisms through alteration of the gut microbiota.

Crotonaldehyde is a ubiquitous hazardous pollutant, present in cigarette smoke and automobile exhaust and is endogenously generated by lipid peroxidation. Most of the current studies focus on its lung toxicity. However, there have been few investigations on the cardiac and renal toxicity caused by crotonaldehyde exposure. We hypothesized that oral intake of crotonaldehyde can cause inflammatory and oxidative/nitrosative damage to the heart and kidneys. Therefore, we treated male rats with crotonaldehyde by gavage at 0, 2.5, 4.5, and 8.5 mg/kg/day for 120 d and evaluated the alterations in histological and serological parameters, oxidative state, and inflammation responses to explore the roles of crotonaldehyde-induced oxidative/nitrosative stress and inflammation in the heart and kidney dysfunction and to explore the relationship between heart and kidney dysfunction. We found that body weight increment, as well as heart and kidney coefficients decreased with an increasing crotonaldehyde dosage. Histological examinations indicated that crotonaldehyde exposure led to focal myocardial necrosis, cardiac fibrosis, renal tubular epithelial cell edema, and renal lymphocyte infiltration. We also assessed the impact of crotonaldehyde treatment on oxidative/nitrosative stress markers, antioxidant enzymes, inflammatory biomarkers, heart/kidney functional markers, and angiotensin II-aldosterone-brain natriuretic peptide (AngII-ALD-BNP) levels. Overall, we found that proinflammatory cytokine and malondialdehyde levels increased in a dose-dependent manner. Furthermore, crotonaldehyde treatment (4.5 and 8.5 mg/kg) significantly prevented the upregulation of antioxidant enzyme activity, thereby increasing oxidative/nitrosative stress (p < 0.05). Moreover, we found that the levels of AngII and ALD increased, whereas the levels of BNP decreased, consistent with heart and kidney dysfunction. Collectively, these results suggest that long-term, low-dose crotonaldehyde exposure leads to an imbalance in AngII-ALD-BNP levels, which mediates cardiac hemodynamic changes causing internal oxidative/nitrosative stress and inflammatory reactions, leading to renal and cardiac dysfunction in male rats.

Fluoride (F) and sulfur dioxide (SO2 ) are the two common environmental contaminants that are associated with neurotoxicity. The present study was conducted to explore individual and combined exposure effects of F and SO2 on histological alteration and DNA damage in rat brain. For this, male Wistar albino rats were exposed to sodium fluoride (100 mg/L NaF) and sulfur dioxide (39.3 mg/m3 ) individually and in combination for 8 weeks. Histological alteration in brain is evaluated by hematoxylin-eosin staining, showed shrunken neurons, darkly stained small nucleus and decreased cell numbers in F and SO2 exposed groups. The effect of F and SO2 on DNA damage was assessed by comet assay. The results showed an increase in ratio of tailing and tail length in F or/and SO2 administered rats. In addition, the proportion of grade II and III were also increased in individual and combined exposed groups. Compared with the individual exposure, the proportion the grade III was significantly high in combined exposure, suggesting a synergistic effect of F and SO2 . These results indicate that the brain was more susceptible to the toxic effects of F and SO2 . And combined exposure to these pollutants can lead more pronounced toxic effects on brain.

Lead is a highly toxic metal and a very potent poison. Lead poisoning is a serious condition but can be treated. Quercetin is a flavonoid with many beneficial uses. The aim of the present study was to investigate the possible modulating action of quercetin as a model of an antioxidant against the toxic effects of lead acetate on liver and kidneys of rats. Rats were randomly divided into four groups: (i) saline group (control); (ii) lead group received i.p. lead acetate (20 mg/kg b.w.); (iii) quercetin group received i.p. quercetin (50 mg/kg b.w.); (iv) lead and quercetin group received i.p. lead acetate (20 mg/kg b.w.) followed by i.p. quercetin (50 mg/kg b.w.) for 4 weeks. The lead concentrations were determined in the liver and kidney tissues. Liver marker enzymes, bilirubin, albumin, total protein, creatinine, uric acid and urea, were assessed in the serum and light microscopic studies were performed. The results showed that lead acetate administration was associated with an increase in serum alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST) activities, total bilirubin, creatinine, uric acid, urea levels. Lead accumulation in kidneys and liver tissues was also found, but were associated with decrease in albumin and total protein in comparison with the respective mean values of the control. Lead acetate caused numerous histological alterations in the liver, including chronic inflammation, bilary hyperplasia, edema, congestion, Kupffer cells hyperplasia and hemosiderosis, and in the kidney, including tubular dilation, atrophy of glomerular tuft, widening of urinary space and mild fibroblast. In contrary, administration of lead acetate along with quercetin partially restored the studied parameters to normal values and improved structure of liver and kidney with significant decreases in the severity of histopathological changes when compared with the lead acetate group. In conclusion, treatment with quercetin may provide a modulating action against the toxic effects induced by lead acetate in the liver and kidney of male rats.

Aphantoxins from Aphanizomenon flos-aquae are frequently identified in eutrophic waterbodies worldwide. These toxins severely endanger environmental safety and human health due to the production of paralytic shellfish poisons (PSPs). Although the molecular mechanisms of aphantoxin neurotoxicity have been studied, many questions remain to be resolved such as in vivo alterations in branchial histology and neurotransmitter inactivation induced by these neurotoxins. Aphantoxins extracted from a naturally isolated strain of A. flos-aquae DC-1 were determined by high performance liquid chromatography. The basic components of the isolated aphantoxins identified were gonyautoxin 1 (GTX1), gonyautoxin 5 (GTX5), and neosaxitoxin (neoSTX), which comprised 34.04, 21.28, and 12.77% of the total, respectively. Zebrafish (Danio rerio) was administrated 5.3 or 7.61mg STX equivalents (eq)/kg (low and high doses, respectively) of the A. flos-aquae DC-1 aphantoxins by intraperitoneal injection. Histological alterations and changes in neurotransmitter inactivation in the gills of zebrafish were investigated for 24h following exposure. Aphantoxin exposure significantly increased the activities of gill alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and resulted in histological alterations in the gills during the first 12h of exposure, indicating the induction of functional and structural damage. Gill acetylcholinesterase (AChE) and monoamine oxidase (MAO) activities were inhibited significantly, suggesting an alteration of neurotransmitter inactivation in zebrafish gills. The observed alterations in gill structure and function followed a time- and dose-dependent pattern. The results demonstrate that aphantoxins or PSPs lead to structural damage and altered function in the gills of zebrafish, including changes in histological structure and increases in the activities of AST and ALT. The inhibition of the activities of AChE and MAO suggest that aphantoxins or PSPs could induce respiratory toxicity in the zebrafish gill. Furthermore, these parameters may be used as bioindicators for investigating aphantoxin exposure and cyanobacterial blooms in nature.