Most tilapias are microphytes, but some prefer higher plants. Ammonia is one of the most important toxic compounds of nitrogen, which is a serious problem in the environment and aquaculture industry. In the present study, juvenile Oreochromis niloticus were exposed to 10, 20, and 30% (96h LC50) of ammonia for two weeks, which are equivalent to 0.9, 1.8, and 2.7 mg / l, respectively. After this period, the fish were anesthetized and blood samples were taken from the caudal stalk with a heparin syringe for evaluating blood indicators. The tissue samples were taken 0.5 cm from the liver, fixed in 10% formalin buffer, and after dehydration with alcohol, clarification with xylol, blocking with paraffin, and cutting 4-6 microns thick with microtome were done. Finally, the stained slides were studied with a light microscope. The results showed phenomena such as hyperemia, nuclear hypertrophy, sinusoidal dilatation, increased melanomacrophage centers, nucleus margination, hepatocyte vacuolation, and cell necrosis in the liver. In the studies of blood serum factors with the increase of ammonia, it has been increased in  AST, ALT, and ALP compared to the control and other groups. Also, as the ammonia concentration increased, the severity of the lesions also increased. Therefore, ammonia causes changes in the structure and activity of metabolic enzymes of the liver, which must be controlled by creating the appropriate ammonia and management conditions in the aquatic environment.

Decabromodiphenyl ethane (DBDPE) is a novel flame retardant that is widely used in plastics, electronic products, building materials and textiles. Our previous studies have revealed the oocyte toxicity of DBDPE, but the effect of DBDPE on preimplantation embryo development has not been reported. Here, we investigated whether and how DBDPE exposure affects preimplantation embryo development. Adult female mice were orally exposed to DBDPE (0, 5, 50, 500 μg/kg bw/day) for 14 days. First, we found that after DBDPE exposure, mice showed obvious circadian rhythm disorder. Moreover, the development of preimplantation embryos was inhibited in DBDPE-exposed mice after pregnancy. Then, we further explored and revealed that DBDPE exposure reduced the endogenous melatonin (MLT) level during pregnancy, thereby inhibiting the development of preimplantation embryos. Furthermore, we discovered that exogenous MLT supplementation (15 mg/kg bw/day) rescued the inhibition of preimplantation embryo development induced by DBDPE, and a mechanistic study demonstrated that exogenous MLT inhibited the overexpression of ROS and DNA methylation at the 5-position of cytosine (5-mC) in DBDPE-exposed preimplantation embryos. Simultaneously, MLT ameliorated the DBDPE-induced mitochondrial dysfunction by increasing the mitochondrial membrane potential (MMP), ATP, and Trp1 expression. Additionally, MLT restored DBDPE-induced changes in zona pellucida (ZP) hardness and trophectoderm (TE) cortical tension. Finally, the protective effect of MLT on embryos ameliorated the adverse reproductive outcomes (dead fetus, fetus with abnormal liver, fetal weight loss) induced by DBDPE. Collectively, DBDPE induced preimplantation embryo damage leading to adverse reproductive outcomes, and MLT has emerged as a potential tool to rescue adverse reproductive outcomes induced by DBDPE.

Although cadmium (Cd) is a toxic heavy metal that reportedly causes liver injury, few studies have investigated biomarkers of Cd-induced liver injury. The purpose of this study is to investigate the role of bile acid (BA) in Cd-induced liver injury and determine reliable and sensitive biochemical parameters for the diagnosis of Cd-induced liver injury. In this study, 48 Sprague-Dawley rats were randomly divided into six groups and administered either normal saline or 2.5, 5, 10, 20, and 40 mg/kg/d cadmium chloride for 12 weeks. A total of 403 subjects living in either a control area (n = 135) or Cd polluted area (n = 268) of Dongdagou-Xinglong (DDGXL) cohort were included, a population with long-term low Cd exposure. The BA profiles in rats' liver, serum, caecal contents, faeces, and subjects' serum were detected using high-performance liquid chromatography-tandem mass spectrometry (HPLC–MS/MS). Changes in rats' and subjects' liver injury indices, rats' liver pathological degeneration, and rats' liver and subjects’ blood Cd levels were also measured. Cadmium exposure caused cholestasis and an increase in toxic BAs, leading to liver injury in rats. Among them, glycoursodeoxycholic acid (GUDCA), glycolithocholic acid (GLCA), taurolithocholic acid (TLCA), and taurodeoxycholate acid (TDCA) are expected to be potential biomarkers for the early detect of Cd-induced liver injury. Serum BAs can be used to assess Cd-induced liver injury as a simple, feasible, and suitable method in rats. Serum GUDCA, GLCA, TDCA, and TLCA were verified to be of value to evaluate Cd-induced liver injury and Cd exposure in humans. These findings provided evidence for screening and validation of additional biomarkers for Cd-induced liver injury based on targeted BA metabolomics.

The experiment was conducted to investigate the effects of Cadmium (Cd) on growth performance, blood biochemical parameters, oxidative stress, hepatocyte apoptosis and autophagy of weaned piglets. A total of 12 healthy weaned piglets were randomly assigned to the control and the Cd group, which were fed with a basal diet and the basal diet supplemented with 15 ± 0.242 mg/kg CdCl₂ for 30 d, respectively. Our results demonstrated that Cd significantly decreased final body weight, average daily feed intake (ADFI), average daily gain (ADG) and increased feed-to-gain (F/G) ratio (P < 0.05). For blood biochemical parameters, Cd treatment significantly decreased the red blood cell (RBC), hemoglobin (HGB), hematocrit (HCT), total protein, albumin, copper content and iron content (P < 0.05). In addition, liver injury was observed in the Cd-exposed group. Our results also demonstrated that Cd exposure contributed to the production of ROS, activated the AMPK/PPAR-γ/NF-κB pathway (increasing the expressions of P-AMPK/AMPK, NF-κB, I-κB-β, COX-2, and iNOS, decreasing the expressions of PPAR-γ and I-κB-α), finally induced autophagy (increasing the expressions of Beclin-1, the ratio of LC3-II/LC3-I and p62), and apoptosis (increasing the expressions of Bax, Bak, Caspase-9, and Caspase-3, decreasing the expression of Bcl-2). Overall, these findings revealed the vital role of AMPK/PPAR-γ/NF-κB pathway in Cd-induced liver apoptosis and autophagy, which provided deeper insights into a better understanding of Cd-induced hepatotoxicity.

Lead is a metal that exists naturally in the Earth's crust and is a ubiquitous environmental contaminant. The alleviation of lead toxicity is important to keep human health under lead exposure. Biosynthesized selenium nanoparticle (SeNPs) and selenium-enriched Lactobacillus rhamnosus SHA113 (Se-LRS) were developed in this study, and their potentials in alleviating lead-induced injury to the liver and intestinal tract were evaluated in mice by oral administration for 4 weeks. As results, oral intake of lead acetate (150 mg/kg body weight per day) caused more than 50 times and 100 times lead accumulation in blood and the liver, respectively. Liver function was seriously damaged by the lead exposure, which is indicated as the significantly increased lipid accumulation in the liver, enhanced markers of liver function injury in serum, and occurrence of oxidative stress in liver tissues. Serious injury in intestinal tract was also found under lead exposure, as shown by the decrease of intestinal microbiota diversity and occurrence of oxidative stress. Except the lead content in blood and the liver were lowered by 52% and 58%, respectively, oral administration of Se-LRS protected all the other lead-induced injury markers to the normal level. By the comparison with the effects of normal L. rhamnosus SHA113 and the SeNPs isolated from Se-LRS, high protective effects of Se-LRS can be explained as the extremely high efficiency to promote lead excretion via feces by forming insoluble mixture. These findings illustrate the developed selenium-enriched L. rhamnosus can efficiently protect the liver and intestinal tract from injury by lead.

Uranium, a radionuclide, is a predominant element utilized for speciality requirements in industrial applications, as fuels and catalyst. The radioactive properties and chemical toxicity of uranium causes a major threat to the ecosystem. The hazards associated with Uranium pollution includes the cancer in bones, liver, and lungs. The toxicological properties of Uranium are discussed in detail. Although there are many methods to eliminate those hazards, this research work is aimed to describe the application of bioremediation methods. Bioremediation methods involve elimination of the hazards of uranium, by transforming into low oxidation form using natural microbes and plants. This study deeply elucidates the methods as bioleaching, biosorption, bioreduction and phytoremediation. Bioleaching process involves bio-oxidation of tetravalent uranium when it gets in contact with acidophilic metal bacterial complex to obtain leach liquor. In biosorption, chitin/chitosan derived sorbents act as chelators and binds with uranium by electrostatic attraction. Bio reduction employs a bacterial transformation into enzymes which immobilize and reduce uranium. Phytoremediation includes phytoextraction and phytotranslocation of uranium through xylems from soil to roots and shoots of plants. The highest uranium removal and uptake reported using the different methods are listed as follows: bioleaching (100% uranium recovery), biosorption (167 g kg⁻¹ uranium uptake), bioreduction (98.9% uranium recovery), and phytoremediation (49,639 mg kg⁻¹ uranium uptake). Among all the techniques mentioned above, bioleaching has been proved to be the most efficient for uranium remediation.

Although Polychlorinated biphenyl (PCB) levels are decreased in the environment, the adverse effects of gestational exposure on the mother and offspring cannot be ignored due to the vulnerability of the fetus. In the present study, pregnant Balb/c mice were administered PCB52 (1 mg/kg BW/day) or corn oil vehicle by gavage until parturition. In the dams, PCB52 caused histopathological changes in the liver, higher serum levels of aminotransferase and alanine aminotransferase, and activated apoptosis and autophagy, suggesting hepatotoxicity. Overexpressed indicators of TLR4 pathway were observed in the liver of PCB52-exposed dams, indicated hepatic inflammation. Moreover, PCB52 exposure weakened the intestinal barrier and triggered inflammatory response, which might contribute to the hepatic inflammation by gut-liver axis. In the pups, prenatal PCB52 exposure affected the sex ratio at birth and reduced birth length and weights. Similar to the dams, prenatal PCB52 exposure induced hepatotoxicity in the pups without gender difference. Consistent with the alteration of gut microbiota, intestinal inflammation was confirmed, accompanying the disruption in the intestinal barrier and the activation of apoptosis and autophagy in the PCB52-exposed pups. Intestinal injury might be responsible for hepatotoxicity at least in part. Taken together, these findings suggested that gestational PCB52 exposure induced hepatic and intestinal injury in both maternal and offspring mice by arousing inflammation.

The Aquidauana River is one of the most important rivers in the Pantanal region, Brazil. However, its waters have been contaminated by nearby anthropogenic activities, threatening native fish species. In this study, our objectives were: 1) to determine the concentrations of Al, As, Cd, Cu, Fe, Mn, Ni, Pb, and Zn in water and sediment samples from the Aquidauana River and to assess the risks posed to aquatic biota; 2) to quantify the concentration of these elements in muscle and liver tissue samples from four native fish species; 3) to evaluate the potential bioaccumulation of inorganic elements in the muscles and liver; and 4) to investigate genotoxicity biomarkers and their association with the inorganic element concentrations present in the muscle tissue. Water and fish samples were collected in November 2020. The concentrations of Al, As, Cd, Cu, Fe, and Pb in the water samples were in disagreement with the Brazilian legislation and presented risks to the aquatic biota. In terms of mixtures of inorganic elements, there was a great increase in the risk to biota. The As concentration did not meet the Brazilian standard for sediments in the sample collected at sampling site 6. The concentrations of Cd and Pb in the muscle tissue of Hypostomus regani, Prochilodus lineatus, Brycon hilarii, and Mylossoma duriventre exceeded the Brazilian standards for human consumption. H. regani showed greater genotoxic damage, and the higher the Al and Fe concentrations in the muscle tissue, the higher the frequencies of lobulated nuclei and nuclear invaginations. Together, our results demonstrate the negative impacts on native fish species from the Aquidauana River contamination and indicate risks to Pantanal biodiversity.