Combined effects of pentachlorophenol and nano-TiO2 with different sizes on antioxidant, digestive, and immune responses of the swimming crab Portunus trituberculatus.

Marine nano-titanium dioxide (nano-TiO2) and pentachlorophenol (PCP) pollution are escalating concerns in coastal areas. This study investigated the combined effects of continuous exposure to nano-TiO2 (25 nm, 100 nm) and PCP (0, 1, 10 µg/L) for 28 days on the antioxidant, digestive, and immune abilities of the swimming crab Portunus trituberculatus. Compared with the control group, the interaction between nano-TiO2 and PCP was significantly higher than exposure to a single stressor, with a pronounced decrease in amylase activity observed due to the reducing nano-TiO2 particle sizes. Resulting in increased MDA and SOD activity. The expression levels of Toll4, CSP3, and SER genes in crab hemolymph showed perturbations following exposure to nano-TiO2 and PCP. In summary, according to the results of CAT, GPX, PES and AMS enzyme activities, it was concluded that compared to the larger particle size (100 nm), the single stress of nano-TiO2 at a smaller particle size (25 nm) and co-stress with PCP have more significant impacts on P. trituberculatus. However, the potential physiological regulation mechanism of the interaction between these pollutants remains elusive and requires further study.

The metabolic activation of pentachlorophenol to chloranil as a potent inhibitor of human and rat placental 3ß-hydroxysteroid dehydrogenases.

Pentachlorophenol (PCP) is a widely used pesticide. However, whether PCP and its metabolite chloranil have endocrine-disrupting effects by inhibiting placental 3ß-hydroxysteroid dehydrogenase 1 (3ß-HSD1) remains unclear. The study used in vitro assays with human and rat placental microsomes to measure 3ß-HSD activity as well as human JAr cells to evaluate progesterone production. The results showed that PCP exhibited moderate inhibition of human 3ß-HSD1, with an IC50 value of 29.83 µM and displayed mixed inhibition in terms of mode of action. Conversely, chloranil proved to be a potent inhibitor, demonstrating an IC50 value of 147 nM, and displaying a mixed mode of action. PCP significantly decreased progesterone production by JAr cells at 50 µM, while chloranil markedly reduced progesterone production at ≥1 µM. Interestingly, PCP and chloranil moderately inhibited rat placental homolog 3ß-HSD4, with IC50 values of 27.94 and 23.42 µM, respectively. Dithiothreitol (DTT) alone significantly increased human 3ß-HSD1 activity. Chloranil not PCP mediated inhibition of human 3ß-HSD1 activity was completely reversed by DTT and that of rat 3ß-HSD4 was partially reversed by DTT. Docking analysis revealed that both PCP and chloranil can bind to the catalytic domain of 3ß-HSDs. The difference in the amino acid residue Cys83 in human 3ß-HSD1 may explain why chloranil is a potent inhibitor through its interaction with the cysteine residue of human 3ß-HSD1. In conclusion, PCP is metabolically activated to chloranil as a potent inhibitor of human 3ß-HSD1.

Co-exposure to pentachlorophenol (PCP) and cadmium (Cd) triggers apoptosis-like cell death in Eschericia coli.

Pentachlorophenol (PCP) - cadmium (Cd) complex pollution has been identified as a form of persistent soil pollution in south China, exerting detrimental impacts on the indigenous soil bacterial communities. Hence, it is worthwhile to investigate whether and how bacterial populations alter in response to these pollutants. In this study, Escherichia coli was used as a model bacterium. Results showed that PCP exposure caused bacterial cell membrane permeability changes, intracellular ROS elevation, and DNA fragmentation, and triggered apoptosis-like cell death at low exposure concentration and necrosis at high exposure concentration. Cd exposure caused severe oxidative damage and cell necrosis in the tested bacterial strain. The co-exposure to PCP and Cd elevated the ROS level, stimulated the bacterial caspase activity, and induced DNA fragmentation, thereby leading to an apoptosis-like cell death. In conclusion, PCP-Cd complex pollution can cause bacterial population to decrease through apoptosis-like cell death pathway. However, it is worth noting that the subpopulation survives under the complex pollution stress.

Pentachlorophenol affects doxycycline and tetracycline resistance genes in soil by altering microbial structure.

Tetracycline antibiotics play a vital role in animal husbandry, primarily employed to uphold the health of livestock and poultry. Consequently, when manure is reintegrated into farmland, tetracycline antibiotics can persist in the soil. Simultaneously, to ensure optimal crop production, organochlorine pesticides (OCPs) are frequently applied to farmland. The coexistence of tetracycline antibiotics and OCPs in soil may lead to an increased risk of transmission of tetracycline resistance genes (TRGs). Nevertheless, the precise mechanism underlying the effects of OCPs on tetracycline antibiotics and TRGs remains elusive. In this study, we aimed to investigate the effects of OCPs on soil tetracycline antibiotics and TRGs using different concentrations of doxycycline (DOX) and pentachlorophenol (PCP). The findings indicate that PCP and DOX mutually impede their degradation in soil. Furthermore, our investigation identifies Sphingomonas and Bacillus as potential pivotal microorganisms influencing the reciprocal inhibition of PCP and DOX. Additionally, it is observed that the concurrent presence of PCP and DOX could impede each other's degradation by elevating soil conductivity. Furthermore, we observed that a high concentration of PCP (10.7 mg/kg) reduced the content of efflux pump tetA, ribosome protective protein tetM, tetQ, and passivating enzyme tetX. In contrast, a low PCP concentration (6.4 mg/kg) only reduced the content of ribosome protective protein tetQ. This suggests that PCP may reduce the relative abundance of TRGs by altering the soil microbial community structure and inhibiting the potential host bacteria of TRGs. These findings have significant implications in understanding the combined pollution of veterinary antibiotics and OCPs. By shedding light on the interactions between these compounds and their impact on microbial communities, this study provides a theoretical basis for developing strategies to manage and mitigate their environmental impact, and may give some information regarding the sustainable use of antibiotics and pesticides to ensure the long-term health and productivity of agricultural systems.

Pentachlorophenol exposure induced neurotoxicity by disrupting citrulline metabolism in larvae and adult zebrafish.

Pentachlorophenol (PCP) is a ubiquitous environmental toxicant with various adverse effects. Although its neurotoxicity has been reported, the underlying mechanism and subsequent detoxification remain unclear. In this study, embryos and adult zebrafish were exposed to PCP to determine its potential neurotoxic mechanism and protective indicators. The survival rate, heart rate, mobility time, active status and moving distance were significantly decreased in larvae after 30 µg/L PCP exposure. Likewise, the mobile time, latency to the first movement, velocity and moving distance of adult zebrafish were significantly reduced by PCP exposure. Untargeted metabolomics analysis of larvae revealed that arginine and proline metabolism was the primary pathway affected by PCP exposure, reflected by increased proline and decreased citrulline (CIT) contents, which were confirmed by quantitative data. PCP exposure suppressed the conversion from arginine to CIT in larvae by downregulating the expression of nos1 and nos2a. Ornithine content was increased in the brains and intestines of adult zebrafish after PCP exposure, which inhibited ornithine catabolism to CIT by downregulating otc, resulting in reduced CIT. Intriguingly, CIT supplementation significantly restored the neurobehavioral defects induced by PCP in larvae and adult zebrafish. CIT supplementation upregulated the expression of ef1α and tuba1 in larvae and inhibited the downregulation of ef1α in the brains of adult zebrafish. Taken together, these results indicated that CIT supplementation could protect against PCP-induced neurotoxicity by upregulating the expression of genes involved in neuronal development and function.

Toxicity assessment and detoxification metabolism of sodium pentachlorophenol (PCP-Na) on marine economic species: a case study of Moerella iridescens and Exopalaemon carinicauda.

Sodium pentachlorophenol (PCP-Na) is widespread in the marine environment; however, its impact on marine organisms remains under-researched. Moerella iridescens and Exopalaemon carinicauda are marine species of economic importance in China and under threat from PCP-Na pollution. Thus, this study aimed to assess the toxicity and detoxification metabolism of PCP-Na on M. iridescens and E. carinicauda. The study revealed that the 96 h median lethal concentration (LC50) of PCP-Na for M. iridescens and E. carinicauda were 9.895 mg/L and 14.143 mg/L, respectively. A species sensitivity distribution (SSD) for PCP-Na was developed specifically for marine organisms, determining a hazardous concentration to 5% of the species (HC5) of 0.047 mg/L. During the sub-chronic exposure period, PCP-Na accumulated significantly in M. iridescens and E. carinicauda, with highest concentrations of 41.22 mg/kg in the soft tissues of M. iridescens, 42.58 mg/kg in the hepatopancreas of E. carinicauda, and only 0.85 mg/kg in the muscle of E. carinicauda. Furthermore, the study demonstrated that detoxifying metabolic enzymes and antioxidant defense system enzymes of E. carinicauda responded stronger to PCP-Na compared to M. iridescens, suggesting that E. carinicauda may possess a stronger detoxification capacity. Notably, five biomarkers were identified and proposed for monitoring and evaluating PCP-Na contamination. Overall, the results indicated that M. iridescens and E. carinicauda exhibit greater tolerance to PCP-Na than other marine species, but they are susceptible to accumulating PCP-Na in their tissues, posing a significant health risk. Consequently, conducting aquatic health risk assessments in areas with potential PCP-Na contamination is strongly recommended.

Nano-TiO2 aggravates the adverse effect of pentachlorophenol on antioxidant and immune response in anti-predatory mussels.

Nano-TiO2 can act as a vector to organic compounds, such as pentachlorophenol (PCP) posing a potential threat to the marine ecosystems. Studies showed that nano pollutant toxicity can be modulated by abiotic factors, but little is known about the potential influence of biotic stressors (such as predators) on the physiological responses to pollutants in marine organisms. We explored the effects of n-TiO2 and PCP on the mussel Mytilus coruscus in the presence of its natural predator, the swimming crab Portunus trituberculatus. Exposure to n-TiO2, PCP, and predation risk showed interactive effects on antioxidant and immune parameters of the mussels. Elevated activities of catalase (CAT), glutathione peroxidase (GPX), acid phosphatase (ACP) and alkaline phosphatase (AKP), suppressed activity of superoxide dismutase (SOD), lower levels of glutathione (GSH) and increased malondialdehyde (MDA) levels indicated dysregulation of the antioxidant system and immune stress induced by single PCP or n-TiO2 exposure. Integrated biomarker (IBR) response values showed the effect of PCP was concentration dependent. Of the two used n-TiO2 sizes (25 and 100 nm), larger particles induced higher antioxidant and immune disturbances indicating higher toxicity possibly due to higher bioavailability. Compared to single PCP exposure, the combination of n-TiO2 and PCP enhanced the imbalance of SOD/CAT and GSH/GPX and led to elevated oxidative lesions and activation of immune-related enzymes. Overall, the combined impacts of pollutants and biotic stress exhibited a greater magnitude of adverse effects on antioxidant defense and immune parameters in mussels. The toxicological effects of PCP were exacerbated in the presence of n-TiO2, and the deleterious impact of these stressors was further amplified under predator-induced risk after prolonged (28 days) exposure. However, the underlying physiological regulatory mechanisms governing the interplay of these stressors and predatory cues on mussels remain elusive, warranting further investigation.

Oral administration of curcumin and gallic acid alleviates pentachlorophenol-induced oxidative damage in rat intestine.

INTRODUCTION: Pentachlorophenol (PCP) is used as pesticide and wood preservative. We have previously shown that PCP causes oxidative damage in rat intestine. AIM: This study aimed to delineate the possible therapeutic potential of curcumin (CUR) and gallic acid (GA) against PCP-induced damage in rat intestine. METHODS: PCP alone group received 125 mg PCP/kg body weight/day orally for 4 days. Animals in combination groups received CUR or GA (100 mg/kg bw) for 18 days and PCP (125 mg/kg bw) for the last four days. Rats were sacrificed and intestinal preparations were analyzed for various parameters. RESULTS: Administration of PCP alone altered the activities of metabolic, antioxidant and brush border membrane enzymes. It also increased DNA-protein crosslinking and DNA-strand scission. Animals in combinations groups showed significant amelioration against PCP-induced oxidative damage. Histological abrasions were seen in PCP alone group which were reduced in the intestines of combination groups. CUR was more effective protectant than GA. CONCLUSIONS: CUR and GA protected rat intestine from PCP-mediated changes in the activities of metabolic, antioxidant and brush border membrane enzymes. They also prevented DNA damage and histological abrasions. The antioxidant character of CUR and GA may be responsible for the diminution of PCP-mediated oxidative damage.

Pentachlorophenol causes redox imbalance, inhibition of brush border membrane and metabolic enzymes, DNA damage and histological alterations in rat kidney.

Pentachlorophenol (PCP) is a synthetic organochlorine compound that is widely used in biocide and pesticide industries, and in preservation of wood, fence posts, cross arms and power line poles. Humans are usually exposed to PCP through air, contaminated water and food. PCP enters the body and adversely affects liver, gastrointestinal tract, kidney and lungs. PCP is a highly toxic class 2B or probable human carcinogen that produces large amount of reactive oxygen species (ROS) within cells. This work aimed to determine PCP-induced oxidative damage in rat kidney. Adult rats were given PCP (25, 50, 100, 150 mg/kg body weight), in corn oil, once a day for 5 days while control rats were given similar amount of corn oil by oral gavage. PCP increased hydrogen peroxide level and oxidation of thiols, proteins and lipids. The antioxidant status of kidney cells was compromised in PCP treated rats while enzymes of brush border membrane (BBM) and carbohydrate metabolism were inhibited. Plasma level of creatinine and urea was also increased. Administration of PCP increased DNA fragmentation, cross-linking of DNA to proteins and DNA strand scission in kidney. Histological studies supported biochemical findings and showed significant damage in the kidneys of PCP-treated rats. These changes could be due to redox imbalance or direct chemical modification by PCP or its metabolites. These results signify that PCP-induced oxidative stress causes nephrotoxicity, dysfunction of BBM enzymes and DNA damage.

Intestinal response of mussels to nano-TiO2 and pentachlorophenol in the presence of predator.

With the development of industry, agriculture and intensification of human activities, a large amount of nano-TiO2 dioxide and pentachlorophenol have entered aquatic environment, causing potential impacts on the health of aquatic animals and ecosystems. We investigated the effects of predators, pentachlorophenol (PCP) and nano titanium dioxide (nano-TiO2) on the gut health (microbiota and digestive enzymes) of the thick-shelled mussel Mytilus coruscus. Nano-TiO2, as the photocatalyst for PCP, enhanced to toxic effects of PCP on the intestinal health of mussels, and they made the mussels more vulnerable to the stress from predators. Nano-TiO2 particles with smaller size exerted a larger negative effect on digestive enzymes, whereas the size effect on gut bacteria was insignificant. The presence of every two of the three factors significantly affected the population richness and diversity of gut microbiota. Our findings revealed that the presence of predators, PCP, and nano-TiO2 promoted the proliferation of pathogenic bacteria and inhibited digestive enzyme activity. This research investigated the combined stress on marine mussels caused by nanoparticles and pesticides in the presence of predators and established a theoretical framework for explaining the adaptive mechanisms in gut microbes and the link between digestive enzymes and gut microbiota.

Study on the toxic effects of sodium pentachlorophenol (PCP-Na) on razor clam (Sinonovacula constricta).

Currently, research on toxic effects of PCP Na is greatly insufficient. The aim of this study is to explore the toxic effects of PCP-Na for better conducting future work on PCP-Na toxicology. For this purpose, S. constricta adults were exposed to PCP-Na for toxicity testing. The results showed that PCP-Na could easily bioaccumulate in S. constricta and significantly affected both phrase I and II metabolism enzymes. Meanwhile, PCP-Na strongly activated antioxidant system and caused PC, LPO and DNA damage. In addition, neurotoxicity and immunotoxicity of PCP-Na was demonstrated in this study. Interestingly, we observed that PCP-Na significantly affected the expression of genes of electron transport chain and induced key enzymes of glycolysis, indicating that PCP-Na may act as an uncoupler of oxidative phosphorylation, interfering with energy supply and causing energy compensation. This study is the first to fully analyze and provide a new perspective on the toxicity of PCP-Na.

Human health ambient water quality criteria and risk assessment of pentachlorophenol in Poyang Lake Basin, China.

Pentachlorophenol (PCP) has been widely used as an insecticide for killing oncomelania (the intermediate host of schistosome) in China and leads to severe environmental contamination. Poyang Lake, as the largest freshwater lake and bird habitat in China, was once a schistosomiasis epidemic area. In this study, the concentrations of PCP in water and aquatic products from Poyang Lake were determined and analyzed, and then the human health ambient water quality criteria (AWQC) was derived based on native parameters of Poyang Lake basin. Finally, a comprehensive analysis of the health risks of drinking water and different types of aquatic products consumption was carried out. The results showed that PCP concentrations were ranged from 0.01 to 0.43 µg/L in surface water and 3.90 to 85.95 µg/kg in aquatic products. Due to the carcinogenicity of PCP, the human health AWQC for PCP are 0.02 µg/L for consumption of water and organisms and 0.03 µg/L for consumption of organisms only. Deterministic and probabilistic risk analysis indicated that the non-carcinogenic risk of PCP were acceptable in Poyang Lake, while the carcinogenic risk cannot be ignored. The health risks of PCP caused by aquatic products consumption were higher than that by drinking water. The percentages of acceptable risk for the population in Poyang Lake Basin were 99.95% at acceptable level of 10-4. Based on the sensitivity analysis, the impact of PCP concentrations on health risk values ranged from 53 to 82%. The study provided valuable information for regional water quality criteria development and water quality assessment.

Variability, determinants, and associations with oxidative stress biomarkers of pentachlorophenol among Chinese pregnant women: A longitudinal study.

Pentachlorophenol (PCP) is ubiquitous and moderately persistent in the environment, and it is an identified human carcinogen. Previous animal experiments indicate that toxic mechanisms of PCP include oxidative stress. However, no epidemiological study has reported the association between PCP exposure and oxidative stress; such association in pregnant women, a vulnerable population, is of particular interest. This study aimed to characterize PCP concentrations in 2304 urine samples from 768 pregnant women, explore its determinants, and evaluate the associations between PCP exposure and three oxidative stress biomarkers across three trimesters. The median concentrations of PCP (100% detected) in the first, second, and third trimester were 0.61, 0.59, and 0.48 ng/mL, respectively, with a significant decrease trend. The intraclass correlation coefficient of specific gravity (SG)-adjusted PCP was 0.26, indicating high variability for PCP across the three trimesters. PCP concentrations were significantly higher in older, pre-pregnancy overweight, multiparous, high-income, and employed women during pregnancy. Urinary PCP was markedly lower in samples collected during spring compared to other seasons. Linear mixed effect models for repeated measures revealed that ln-transformed SG-adjusted PCP was significantly associated with increased 8-hydroxy-2'-deoxyguanosine (8-OHdG; percent change [%Δ] caused by each interquartile range increase of PCP: 46.2, 95% confidence interval [CI]: 40.2, 52.5) and 8-hydroxyguanosine (8-OHG;%Δ [95% CI]: 44.8 [40.1, 49.8]), but the positive association with 4-hydroxy2-nonenal-mercapturic acid (HNE-MA) was not significant. PCP was also positively associated with increased 8-OHdG and 8-OHG in each trimester using general linear models, and its associations with HNE-MA were only significant at T1 (%Δ [95% CI]: 19.1 [1.05, 40.3]) and T2 (%Δ [95% CI]: 12.6 [0.32, 26.3]). Our findings provide valuable information about PCP exposure characteristics during pregnancy and the potential effects of PCP exposure on oxidative stress in pregnant women.

Immunotoxicity of pentachlorophenol to a marine bivalve species and potential toxification mechanisms underpinning.

The ubiquitous presence of pentachlorophenol (PCP) in ocean environments threatens marine organisms. However, its effects on immunity of marine invertebrates at environmentally realistic levels are still largely unknown. In this study, the immunotoxicity of PCP to a representative bivalve species was evaluated. In addition, its impacts on metabolism, energy supply, detoxification, and oxidative stress status were also analysed by physiological examination as well as comparative transcriptomic and metabolomic analyses to reveal potential mechanisms underpinning. Results illustrated that the immunity of blood clams was evidently hampered upon PCP exposure. Additionally, significant alterations in energy metabolism were detected in PCP-exposed clams. Meanwhile, the expressions of key detoxification genes and the in vivo contents (or activity) of key detoxification enzymes were markedly altered. Exposure to PCP also triggered significant elevations in intracellular ROS and MDA whereas evident suppression of haemocyte viability. The abovementioned findings were further supported by transcriptomic and metabolomic analyses. Our results suggest that PCP may hamper the immunity of the blood clam by (i) constraining the cellular energy supply through disrupting metabolism; and (ii) damaging haemocytes through inducing oxidative stress. Considering the high similarity of immunity among species, many marine invertebrates may be threatened by PCP, which deserves more attention.

Pentachlorophenol mediated regulation of DAMPs and inflammation: In vitro study.

Pentachlorophenol (PCP) was once a widely employed organochlorine pesticide and wood preservative in United States. Due to its toxicity, the U.S. Environmental Protection Agency has classified it as a restricted-use pesticide and established as a liver carcinogen. Earlier reports have indicated increased production of inflammatory mediators like IL-1ß and TNF-α by immune cells, including NK cells, lymphocytes, or monocytes -on PCP exposure. Yet, there is only scant information available regarding the detailed molecular mechanisms affected by acute or chronic exposure of humans to PCP. Considering this, we examined PCP-induced inflammation and downstream signaling events in-(a) human lung adenocarcinoma cells (A549) with type II alveolar epithelial characteristics; and (b) human liver carcinoma cells (HepG2). Treatment of these cells with 1 µM and 10 µM concentration of PCP for 24 h duration resulted in a significant induction of cytokines/chemokines including IL-1ß, IL-6, TNF-α, IL-8, CCL2, and CCL5. Assessment of mRNA expression showed upregulated levels of danger-associated molecular patterns (DAMPs)-high mobility group box-1 (HMGB1) and heat shock protein 70 (Hsp70) as well as TLR-4 receptor in PCP-challenged cells. Increased expression of transcription factors-NF-κB and STAT3 provide further insight into the molecular mechanisms underlying PCP-induced toxicity/pathology. Interestingly, antibody-mediated neutralization of DAMPs abrogates PCP-mediated transcriptional induction of cytokines, chemokines and transcription factors in HepG2 and A549 cells. Overall, our findings demonstrate the important role of DAMPs in PCP-induced inflammatory responses.

Toxicity Analysis of Pentachlorophenol Data with a Bioinformatics Tool Set.

Rapid progress in technologies opened the new era of computer-leaded analytics, leaving humans more space for experimental design and decision making. Here we demonstrate the machine learning analysis workflow represented by spectral clustering, elucidation of evolutionary conserved transcription regulation, and network analysis using reverse engineering. Analysis of genes induced by the Pentachlorophenol toxic chemical revealed two subnetworks, one orchestrated by Interferon and another by Nuclear receptor factor 2 (NRF2) gene. Furthermore, network-inference based analysis identified a gene network module composed of genes associated with interferon signaling and their regulatory interaction with downstream genes, especially TRIM family proteins involved in responses of innate immune systems.

Pentachlorophenol has significant adverse effects on hematopoietic and immune system development in zebrafish (Danio rerio).

In November 2018, the Camp Fire devastated the mountain community of Paradise, CA. The burning of plastic pipes, wiring, construction materials, paint, and car batteries released toxic chemicals into the environment, contaminating the air, soil, and local waterways. Examples of toxins that were identified in the creeks and waterways in and around Paradise included pentachlorophenol (PCP), chrysene, and polyaromatic hydrocarbons. The effects of some of these chemicals on embryonic development, hematopoiesis (blood formation), and the immune system have not been thoroughly studied. Defining safe levels and the long-term effects of exposure is imperative to understanding and mitigating potential negative future outcomes. To perform these studies, we utilized zebrafish (Danio rerio), a commonly used vertebrate model system to study development. We observed the adverse effects of PCP on the development of zebrafish by using fluorescence microscopy, and saw that increased concentrations of PCP decreased the numbers of normal red blood cells and myeloid cells. Additionally, we observed that animal survival decreased in response to increasing concentrations of PCP. Furthermore, the prevalence of characteristic physical deformities such as tail curvature were greater in the treatment groups. Lastly, runx1, cmyb, and cd41 expression was reduced in fish treated with PCP. These results suggest that PCP has a previously underappreciated effect on blood and immune cell development and future studies should be performed to determine the molecular mechanisms involved.

3,4-Dihydroxybenzaldehyde attenuates pentachlorophenol-induced cytotoxicity, DNA damage and collapse of mitochondrial membrane potential in isolated human blood cells.

Pentachlorophenol (PCP) is a chlorophenolic compound that is widely used as pesticide, biocide and as a wood preservative to treat utility poles and wharf pilings. PCP is rapidly absorbed through the gastrointestinal tract and enters the blood where it generates active oxygen species in target cells. We have, therefore, examined the protective effect of plant antioxidant 3,4-dihydroxybenzaldehyde (DHB) against PCP-induced cyto-and geno-toxicity in human red blood cells (RBC) and lymphocytes, respectively. Human RBC were incubated at 37°C with 0.75 mM PCP, either alone or in presence of different concentrations of DHB (0.05-2.0 mM). Several biochemical parameters were determined in whole cells and hemolysates. Incubation of RBC with PCP alone increased the formation of reactive oxygen and nitrogen species (ROS and RNS) that resulted in oxidation of proteins, lipids, cellular thiols and plasma membrane damage. The antioxidant defense system was impaired and glucose metabolism was inhibited. However, prior treatment of RBC with DHB lowered ROS and RNS generation and attenuated PCP-induced oxidative damage of cell components. DHB alone enhanced electron transport by the plasma membrane redox system and also prevented its inhibition by PCP. DHB significantly prevented PCP-induced transformation of RBC morphology from normal biconcave shape to spherocytes, spiculated acanthocytes and echinocytes. DHB protected human lymphocytes from PCP-induced DNA damage and strand breaks, lysosomal membrane damage and collapse of the mitochondrial membrane potential. These results show that DHB mitigates PCP-induced cytotoxicity and can potentially function as a chemoprotective agent against the harmful effects of PCP and possibly other chlorophenols.

Multidimensional bioresponses in nematodes contribute to the antagonistic toxic interaction between pentachlorophenol and TiO2 nanoparticles in soil.

Interactions between nanomaterials (NMs) and coexisting contaminants are important contributors to their joint biological effects, while the reverse actions of bioresponses in determining the toxic interaction between NMs and contaminants were rarely understood. Here, we investigated the toxic interaction and mechanism between TiO2 NMs (nTiO2) and pentachlorophenol (PCP) in soil using the model nematode (Caenorhabditis elegans). PCP (0.5-50 mg/kg) and nTiO2 (50-5000 mg/kg) co-exposures induced antagonistic effects on the survival, growth, and locomotion of nematodes, and the levels of ultrastructural damage and oxidative stress exhibited consistent alterations. Soil PCP concentrations changed insignificantly after the single or combined exposures, indicating a negligible direct interaction between PCP and nTiO2 under the soil condition. Transcriptomic analysis revealed that after 50 mg/kg PCP exposure, half of differentially expressed genes were involved in epidermal collagen synthesis, while the PCP-nTiO2 co-exposure particularly activated genes related to antistress responses and the positive regulation of physiological functions. Further biochemical analysis demonstrated the antagonistic interactions were derived from two aspects: 1) PCP-induced epidermal collagen incrassation lowered the bioaccumulation and toxicity of nTiO2; 2) nTiO2-activated glutathione detoxification pathway alleviated PCP-induced toxicity. These findings highlight the key role of bioresponses in determining toxic interactions between NMs and co-contaminants.

Ecotoxicological risk assessment of pentachlorophenol, an emerging DBP to plants: evaluation of oxidative stress and antioxidant responses.

Chlorophenols are not only noticed in an effluvium of industries but also can emerge from the water treatment plants for domestic supply which poses a high threat for crop production and human health. Therefore, research on their risks to ecosystem and human health via ecotoxicological tests to derivate permissible environmental contaminant concentrations is necessary. The chlorophenols produced in the course of chlorination of potable water is an outcome of natural carboxylic acids/organic material and those chlorophenols occurred as emerging disinfection byproducts (EDBPs). Among chlorophenols, pentachlorophenol (PCP) has been recently identified as one of the important EDBPs. The main objective was to evaluate the PCP-induced genotoxicity and the oxidative damage in two plant species, i.e., Allium cepa and Vigna radiata. Genotoxicity of PCP was examined at three selected concentrations based on EC50 (half-maximal effective concentrations) values in both the plants along with the defense mechanism. EC50 value for A. cepa and V. radiata was 0.7 mg/L and 35 mg/L. Root length inhibition, DNA laddering, lipid peroxidation, H2O2 content, and antioxidant enzymatic assays evaluated revealed a dose-dependent response. PCP influenced defense enzyme glutathione peroxidase (GPX) and ascorbate peroxidase (APX) action in both plants and showed deprivement of catalase (CAT) with the increase of PCP concentrations. PCP-invaded toxicity management by these plants implied that A. cepa is more sensitive than V. radiata regarding PCP-induced toxicity.