Ciprofloxacin (Cipro) is commonly detected in water worldwide, however, the ecotoxicological effects to aquatic biota is still not fully understood. In this study, using multiple biomarkers, it was investigated sublethal effects of short-term exposure to Cipro concentrations (1, 10 and 100 μg.L⁻¹) in the Neotropical catfish Rhamdia quelen compared to non-exposure treatment (Control). After 96 h of exposure, the fishes were anesthetized for blood collection to hematological and genotoxicity biomarkers analysis. After euthanasia, the brain and muscle were sampled for biochemical biomarkers analyses. Gills, liver and posterior kidney for genotoxicity, biochemical and histopathological biomarkers analysis and anterior intestine for histopathological biomarkers analysis. Genotoxicity was observed in all tissues, regardless of the Cipro concentrations. Hematological alterations, such as reduction of the number of erythrocytes and leucocytes, as well as in hematocrit concentration and histopathological damages, such as reduction of microridges in gill epithelium and necrosis in liver and posterior kidney, occurred mainly at 100 μg.L⁻¹. In addition, at 100 μg.L⁻¹, Cipro increased antioxidant system activity (Catalase in liver and posterior kidney). These results demonstrated that under short-term exposure, Cipro causes toxic effects in R. quelen that demands attention and surveillance of environmental aquatic concentrations of this antibiotic.

Bisphenol S is an endocrine disruptor exhibiting metabolic disturbances, especially following perinatal exposures. To date, no data are available on the obesogen effects of BPS in a mutligenerational issue.We investigated obesogen effects of BPS in a multigenerational study by focusing on body weight, adipose tissue and plasma parameters in male and female mice.Pregnant C57BL6/J mice were exposed to BPS (1.5 μg/kg bw/day ie a human equivalent dose of 0.12 μg/kg bw/day) by drinking water from gestational day 0 to post natal day 21. All offsprings were fed with a high fat diet during 15 weeks. Body weight was monitored weekly and fat mass was measured before euthanasia. At euthanasia, blood glucose, insuline, triglyceride, cholesterol and no esterified fatty acid plasma levels were determined and gene expressions in visceral adipose tissue were assessed. F1 males and females were mated to obtain the F2 generation. Likewise, the F2 mice were cross-bred to obtain F3. The same analyses were performed.In F1 BPS induced an overweight in male mice associated to lipolysis gene expressions upregulation. In F1 females, dyslipidemia was observed. In F2, BPS exposure was associated to an increase in body weight, fat and VAT masses in males and females. Several plasma parameters were increased but with a sex related pattern (blood glucose, triglycerides and cholesterol in males and NEFA in females). We observed a down-regulation in mRNA expression of gene involved in lipogenesis and in lipolysis for females but only in the lipogenesis for males. In F3, a decrease in VAT mass and an upregulation of lipogenesis gene expression occurred only in females.BPS perinatal exposure induced sex-dependent obesogen multigenerational effects, the F2 generation being the most impacted. Transgenerational disturbances persisted only in females.

Maternal nicotine exposure during lactation induces liver damage in adult male rats. However, the mechanism in males is unknown and females have not been tested. Here, we determined the liver lipid composition and lipogenic enzymes in male and female offspring at two ages in a model of postnatal nicotine exposure. Osmotic minipumps were implanted in lactating Wistar rat dams at postnatal day (PND) 2 to release 6 mg/kg/day of nicotine (NIC group) or saline (CON group) for 14 days. Offspring received a standard diet from weaning until euthanasia at PND120 (1 pup/litter/sex) or PND180 (2 pups/litter/sex). At PND120, NIC males showed lower plasma triglycerides (TG), steatosis degree 1, higher hepatic cholesterol (CHOL) ester, free fatty acids, monoacylglycerol content as well as acetyl-coa carboxylase-1 (ACC-1) and fatty acid synthase (FAS) protein expression in the liver compared to CON males. At this age, NIC females had preserved hepatocytes architecture, higher plasma CHOL, higher CHOL ester and lower total CHOL content in the liver compared to CON females. At PND180, NIC males showed steatosis degrees 1 and 2, higher TG, lower free fatty acids and total CHOL content in the liver and an increase in ACC-1 hepatic protein expression. NIC females had higher plasma TG and CHOL levels, no change in hepatic morphology, lower CHOL ester and free fatty acids in the liver, which also showed higher total ACC-1 and FAS protein expression. Maternal nicotine exposure induces long-term liver dysfunction, with an alteration in hepatic cytoarchitecture that was aggravated with age in males. Concerning females, despite unchanged hepatic cytoarchitecture, lipid metabolism was compromised, which deserves further attention.

Methods to assess the effects of contaminants on marine organisms typically involve euthanasia to obtain samples, but less invasive techniques may be more appropriate for working with threatened species. In this study, were assessed the biological responses of crabs exposed to microplastics and contaminants of emerging concern. Biochemical and cellular effects (lipid peroxidation, DNA damage, cholinesterase activity, and lysosomal membrane stability) in hemolymph were analyzed in a kinetic study, at 3 and 7 days, in U. cordatus exposed to microplastics spiked with Triclosan (TCS) or 17α-Ethynylestradiol (EE2). The results showed that the contaminants were produced toxic effects in the crabs exposed either to the microplastics alone (oxidative stress, genotoxicity, and neurotoxicity), or to microplastics with TCS or EE2 adsorbed (neurotoxic and cytotoxic). The present study showed the responsiveness of non-lethal analyzes to understanding the biological effects of combined exposure to microplastics and chemical pollution.

This study aimed to investigate the possible mechanisms of environmental metal pollutant lead (Pb)-induced apoptosis in chicken. Forty 8-day-old healthy chickens were randomly assigned to two groups (n = 20/group) after raising standard commercial diet and drinking water for 1 week: including control group and Pb group ((CH₃COO)₂Pb 350 mg/L of drinking water); the chickens were given euthanasia and collected livers at 90 days. A significant increase of apoptosis rate were found in Pb group and Pb induced obvious ultrastructural changes of chicken liver. The mRNA levels of glycometabolism key enzymes were significantly lower in Pb group than those in controls. Higher levels of malondialdehyde (MDA) and nitric oxide (NO) were observed in Pb group; the activities of antioxidant enzymes and ATPases were significantly lower in Pb group than those in controls, while the inducible nitric oxide synthase (iNOS) activity was on the contrary. The mRNA and protein levels of pro-apoptotic genes were all lower in Pb group than those in controls. Altogether, Pb-induced mitochondrial swelling and nuclear chromatin condensation, oxidative stress, energy metabolism disorder, thereby lead to apoptosis via mitochondrial pathway in chicken liver, suggesting that Pb-induced mitochondrial pathway apoptosis plays an important role in the mechanisms of Pb cytotoxicity to chicken liver.

Although tannery effluents are known for being highly toxic to organisms, reports about the effects of the intake of these xenobiotics on experimental mammal models are recent. Studies about the damages the chronic intake of these effluents can cause in the liver of outbred mice remain an unexplored field. Thus, the aim of the present study is to assess (histological) the hepatic condition of Swiss mice (outbred strain) chronically exposed to the intake of different raw tannery effluent concentrations diluted in water for 150 days. Accordingly, the mice (males and females) were divided in the following groups: control group—animals treated with drinking water, only; and groups 5 and 10%—treated with raw tannery effluent diluted in water. After exposure, the animals were subjected to euthanasia for liver fragment sample collection and histological analysis, respectively. Moderate hydropic degeneration was observed in the centrilobular regions of the liver of mice exposed to 5 and 10% tannery effluent, as well as greater amounts of hepatocytes presenting karyomegaly and necrotic hepatocytes, and a smaller amount of Kuffer cells in the liver of mice exposed to the xenobiotic. Finally, animals exposed to 10% tannery effluent showed mild hyperplasia of the bile ducts in the portal areas and fibroblast proliferation around the bile ducts, thus suggesting a fibrous process. Except for the frequency of hepatocytes presenting karyomegaly (lower in females), the herein observed hepatic changes were similar in male and female Swiss mice. Accordingly, the present data support the hypothesis that the chronic intake of tannery effluent by outbred mice (Swiss) causes damages in the liver, a fact that broadens the knowledge about the toxic potential of this pollutant, which goes beyond that of C57Bl/6J male mice (inbred strain).