Mixed Exposure of Persistent Organic Pollutants Alters Oxidative Stress Markers and Mitochondrial Function in the Tail of Zebrafish Depending on Sex

Persistent organic pollutants (POPs) are lipid-soluble toxins that are not easily degraded; therefore, they accumulate in the environment and the human body. Several studies have indicated a correlation between POPs and metabolic diseases; however, their effects on mitochondria as a central organelle in cellular metabolism and the usage of mitochondria as functional markers for metabolic disease are barely understood. In this study, a zebrafish model system was exposed to two subclasses of POPs, organochlorine pesticides (OCPs) and polychlorinated biphenyls (PCBs), under two different conditions (solitary OCPs or OCPs with PCBs (Aroclor 1254)), and changes in the oxidative stress marker levels and mitochondrial enzyme activities in the electron transport chain of the tail were measured to observe the correlation between POPs and representative biomarkers for metabolic disease. The results indicated different responses upon exposure to OCPs and OCPs with Aroclor 1254, and accelerated toxicity was observed following exposure to mixed POPs (OCPs with Aroclor 1254). Males were more sensitive to changes in the levels of oxidative stress markers induced by POP exposure, whereas females were more susceptible to the toxic effects of POPs on the levels of mitochondrial activity markers. These results demonstrate that the study reflects real environmental conditions, with low-dose and multiple-toxin exposure for a long period, and that POPs alter major mitochondrial enzymes’ functions with an imbalance of redox homeostasis in a sex-dependent manner.

Leaching Rate of Polychlorinated Biphenyls (PCBs) from Marine Paint Chips

Polychlorinated biphenyls (PCBs) were added to certain marine vessel bottom paints as a plasticizer to improve the adhesion and durability of the paint. The most common PCB formulation used to amend such paints was Aroclor 1254. Fugitive Aroclor-containing paint chips generated from vessel maintenance and repair operations represent a potential source of PCB contamination to sediments. Limited published studies indicate that Aroclor-containing paint is largely inert and exhibits low PCB leaching into water; however, the rate and degree of leaching of PCBs from paint chips have not been directly studied. This laboratory-based study evaluated the rate and extent of leaching of PCBs from paint chips into freshwater. The results of this investigation demonstrate that the rate of PCB dissolution from paint chips decreased rapidly and exponentially over time. Based on this study, it is estimated that the rate of leaching of PCBs from paint chips would cease after approximately 3 years of exposure to water. When all leachable PCBs were exhausted, it is estimated that less than 1% of the mass of PCBs in the paint chips was amenable to dissolution. The results of this experiment suggest that Aroclor-containing paint chips found in sediments are likely short-term sources of dissolved-phase PCB to pore or surface waters and that the majority of the PCBs in paint chips remain in the paint matrix and unavailable for partitioning into water. Graphic Abstract

Sex dependent action of Aroclor 1254 on basal and sGnRHa-stimulated secretion of LH from the pituitary cells of common carp, Cyprinus carpio L.

Polychlorinated biphenyls (PCBs) affect the hypothalamic-pituitary-gonadal axis in many vertebrates, changing the hormonal regulation of reproduction. To identify one of the possible sites of action of PCBs on gonadotropin release in common carp, the direct effects of Aroclor 1254 on luteinizing hormone (LH) secretion from dispersed pituitary cells were investigated. Pituitary cells were obtained from sexually mature male and female common carp (Cyprinus carpio L.) at the time of natural spawning. The cells were incubated with different concentrations of Aroclor 1254 (5, 10, 50 and 100 ng mL−1 medium) and/or salmon gonadotropin-releasing hormone analogue (sGnRHa) at a concentration of 10−8 M. LH levels were measured in the cultured medium by the ELISA method after 10 hours of cell incubation. Incubation of male pituitary cells in the presence of tested concentrations of Aroclor did not change the basal LH secretion to the media. In the female pituitary cell incubations Aroclor (5, 10 and 100 ng mL−1 medium) caused a significant increase in LH concentrations in comparison to control incubations. In the case of sGnRHa-stimulated LH secretion in incubations of cells of both sexes, all the concentrations of Aroclor significantly stimulated LH release and potentiated stimulatory effects of sGnRH analogue. These results indicate that endocrine disrupters, such as Aroclor 1254, may affect reproduction in fish, acting also directly on gonadotrophs at the level of the pituitary gland, changing LH secretion.

Renal changes and apoptosis caused by subacute exposure to Aroclor 1254 in selenium-deficient and selenium-supplemented rats

Aroclor 1254 (A1254), a mixture of polychlorinated biphenyls, exerts hepatic, renal, and reproductive toxicity in rodents. This study aimed to determine a protective role of selenium on histopathological changes, oxidative stress, and apoptosis caused by A1254 in rat kidney. It included a control group, which received regular diet containing 0.15 mg/kg Se (C), a Se-supplemented group (SeS) receiving 1 mg/kg Se, a Se-deficient group (SeD) receiving Se-deficient diet of ≤0.05 mg/kg Se, an A1254-treated group (A) receiving 10 mg/kg of Aroclor 1254 and regular diet, an A1254-treated group receiving Se-supplementation (ASeS), and an A1254-treated group receiving Se-deficient diet (ASeD). Treatments lasted 15 days. After 24 h of the last dose of A1254, the animals were decapitated under anaesthesia and their renal antioxidant enzyme activities, lipid peroxidation (LP), glutathione, protein oxidation, and total antioxidant capacity levels measured. Histopathological changes were evaluated by light and electron microscopy. Apoptosis was detected with the TUNEL assay. Kidney weights, CAT activities, and GSH levels decreased significantly in all A1254-treated groups. Renal atrophic changes and higher apoptotic cell counts were observed in the A and ASeD groups. Both groups also showed a significant drop in GPx1 activities (A – 34.92 % and ASeD – 86.46 %) and rise in LP (A – 30.45 % and ASeD – 20.44 %) vs control. In contrast, LP levels and apoptotic cell counts were significantly lower in the ASeS group vs the A group. Histopathological changes and renal apoptosis were particularly visible in the ASeD group. Our findings suggest that selenium supplementation provides partial protection against renal toxicity of Aroclor 1254.