Toxicity Of Nonylphenol Research Articles

Nonylphenol Toxicity: Exposure, Mode of Action, Toxic Effects

Nonylphenol Toxicity: Exposure, Mode of Action, Toxic Effects

Alkylphenols cause cytotoxicity and genotoxicity induced by oxidative stress in RTG-2 cell line

Alkylphenols ethoxylates are industrial surfactants, and the release in the environmental matrices produces degraded products, of which nonylphenol (NP) and octylphenol (OP) were the most common. They can be classified as endocrine disruptors since the estrogenic potential is widely recognized, but some others toxic aspects are in discussion. This study aimed to evaluate the toxicity of NP, OP, and mixtures of both through cellular, biochemical and genetic biomarkers in fish gonadal cell line RTG-2 exposed to nominal concentrations of 0.05; 0.5; 5; 50, and 100 μg mL−1 of each chemical and their mixtures of 0.05, 0.5; 5 μg mL−1 concentrations. After 24 h, the cells were collected for cytotoxic (neutral red – NR; crystal violet - CV, resazurin assay – RA and lactate-dehydrogenase - LDH), antioxidant system (glutathione-s-transferase – GST; superoxide-dismutase – SOD; glutathione-peroxidase – GPx and malondialdehyde – MDA) and genotoxic assays (alkaline comet assay and Fpg-modified alkaline comet assay). The chemicals and their mixtures were cytotoxic at 50 and 100 μg mL−1, in general aspect, but LDH showed cytotoxicity since 0.05 μg mL−1. The GST and SOD showed an activity increase trend in most tested groups, while GPx decreased at 5 μg mL−1 of the mixture. The MDA increase in all groups resulted in lipid peroxidation. The reactive oxygen species caused DNA damage for all groups. The tested chemicals and concentrations have been found in the freshwater systems. They can induce cell toxicity in several parameters that could impair the gonadal tissues considering the RTG-2 responses.

Nonylphenol inhibited HIF-1alpha regulated aerobic glycolysis and induced ROS mediated apoptosis in rat Sertoli cells

Nonylphenol (NP) is an endocrine disruptor with reproductive toxicity, which can induce apoptosis of Sertoli cells (SCs). SCs have a high aerobic glycolytic flux to ensure sufficient lactate for germ cells as central energy metabolite, and hypoxia-inducible factors 1alpha (HIF-1α) is a major regulator of glycolysis. This study aimed to investigate whether NP can alter HIF-1α-regulated aerobic glycolysis metabolism and thus induce apoptosis in rat SCs. The results revealed that cell viability, intracellular and extracellular lactate levels, the expression of Hk2, Ldha and Mct4, and the protein levels of HIF-1α, HK2, LDHA and MCT4 were decreased significantly when rat SCs exposed to 20 and 30 μM NP for 24 h. Compared with the 30 μM NP group, the protein levels of HIF-1α, HK2 and LDHA, the expression of Hk2 and Ldha and intracellular lactate levels were increased in 30 μM NP and 125 μM cobalt chloride (CoCl2, inhibitor of HIF-1α proteasome-mediated degradation) co-treated group. Furthermore, the elevation of reactive oxygen species (ROS) and apoptosis induced by 30 μM NP were also reversed. In summary, exposure to NP inhibited the ability of SCs to produce and secrete lactate. Meanwhile, NP exposure could lead to a decrease in HIF-1α thereby inhibiting aerobic glycolysis in rat SCs, disrupting intracellular homeostasis and further inducing ROS-mediated apoptosis. This research is the first to explore the NP toxicity on SCs function with respect to nutrition support to germ cells, and provide new evidence on the inhibition of aerobic glycolysis inducing ROS-mediated apoptosis in SCs.

Separate and combined effects of cadmium (Cd) and nonylphenol (NP) on growth and antioxidative enzymes in Hydrocharis dubia (Bl.) Backer.

Cadmium (Cd) is considered a priority pollutant, and nonylphenol (NP) is a common organic pollutant in water environments. However, the ecological risks of combined Cd and NP pollution have not been fully elucidated. In this study, the effects of Cd, NP, and Cd-NP on the growth and physiology of Hydrocharis dubia (Bl.) Backer were studied. The results indicated that Cd-NP joint toxicity is concentration-dependent. The joint toxicity of Cd and NP on H. dubia was antagonistic when the concentrations of Cd + NP were 0.01 + 0.1/1mg/L. At 0.5 + 0.1/1mg/L, Cd and NP had a strong synergistic effect on H. dubia. In addition, plant growth was significantly inhibited, and the chlorophyll contents were significantly reduced under Cd, NP, or Cd-NP exposure. The plant's antioxidant enzyme system was destroyed. The activities of superoxide dismutase (SOD) and catalase (CAT) were significantly decreased under NP-only exposure. The activity of SOD was significantly decreased under Cd-only and under joint exposure. Compound pollution exceeded the oxidative defense capacity of the plants, so the H2O2 content increased significantly. Our results indicated that the ecotoxicity of NP combined with Cd may be exacerbated in aquatic environments and cause obvious damage to H. dubia.

Palliative effect of dietary common sage leaves against toxic impacts of nonylphenol in Mirror carp (Cyprinus carpio var specularis): Growth, gene expression, immune-antioxidant status, and histopathological alterations

Nonylphenol (NP) is a common toxicant that constitutes a potential hazard to the aquatic system. This study assessed the protective role of Salvia officinalis leaves powder (SOLP) against NP toxicity. We addressed mortalities, growth retardation, hepato-renal dysfunction, immune-antioxidant suppression, histopathological degeneration, and gene down-regulation induced by NP-toxicity. And the potential activity of SOLP against these negative impacts in Mirror carp (Cyprinus carpio var specularis). Acute toxicity assay (static 96-h) was primarily performed to investigate the 96-h LC50 of NP in C. carpio and it was recorded at 1.01 mg/L reckoned by Finney probit analysis. Fish (N = 240) were assigned to 4 treatments for 2 months. The first (control) and the second (SOLP) groups were fed on basal diets that were enriched with 0.0 and 4 g/kg of diet SOLP without NP exposure. The third (NP) and fourth (SOLP+NP) groups were provided with the same diets plus exposed to 1/10 of the 96 h-LC50 of NP (0.1 mg/L). The outcomes revealed that NP induced higher mortalities (46), significantly (p < 0.05) reduced growth, serum immune (nitric oxide and immunoglobulin M), and antioxidants (glutathione peroxidase and catalase) values. Moreover, down-regulation of immune-related genes (interleukin 6 and tumor necrosis factor-alpha) in the head kidney, and gills was observed in the NP group. However, noticeable augmented levels of serum oxidant (malondialdehyde), liver enzymes (Alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase); and kidney biomarkers (creatinine and urea) were recorded in NP group. Extensive pathology revealed that NP induced damage to hepatocytes and renal epithelium and mononuclear cells infiltrations in hepato-renal tissues. Dietary intervention with SOLP reduced mortalities (20 %), restored the reduction in the growth and biochemical indicators, and recovered the histopathology, and gene down-regulation produced by NP. Accordingly, the current study recommended SOLP as a valuable dietary additive in aquaculture owing to its mitigating impacts against NP by improving growth and immune-antioxidant status and regenerating the histological structure with a better gene expression.

Transcriptional expression analysis reveals multiple effects of nonylphenol exposure on scallop immune system

Nonylphenol (NP) is an endocrine disruptor and environmental hormone representing alkylphenol compounds. Marine mollusks are an important source of protein for people worldwide. Many researchers have begun to study the effect of NP on marine mollusks immune system in view of its toxicity; however, the underlying molecular mechanisms require in-depth analysis. In this study, we focused on the transcriptional expression change of immune-related genes and antioxidant enzymes activities variation after NP exposure in a marine bivalve mollusk, Chlamys farreri, to explore the immunomodulatory capacity of NP in marine mollusks. We identified MAVS (Mitochondrial antiviral signaling protein), a key adaptor molecule in the RLR (RIG-I like receptor) pathway, and studied the expression of multiple immune-related genes in response to different concentrations of NP. The key genes involved in RLR/TLR (Toll like receptor) innate immune pathway, apoptosis, and cellular antioxidation mechanism were investigated. Changes in the enzymatic activities of scallop antioxidant enzymes after NP exposure were also examined. The results revealed that the genes expression and the antioxidant enzymes activities show significant changes, thus proving that NP stimulation affects the scallop immune system. Our research results demonstrate the immunomodulatory capacity of NP in marine bivalve mollusks and lay the foundation for further in-depth analysis of the molecular mechanism of NP toxicity.

Mycelium polysaccharides of Macrolepiota procera alleviate reproductive impairments induced by nonylphenol.

Nonylphenol (NP) exposure has become a crucial inducement of male reproductive disorders in the world. Therefore, it is urgent to seek solutions to alleviate the toxicity of NP. This study was oriented toward studying the protective effects of Macrolepiota procera mycelium polysaccharides (MMP) on NP-induced reproductive impairments. After NP administration, declined sperm amounts and testis index, increased the deformity rate of sperms, aberrant hormone secretion and testicular pathological injury were observed, corporately leading to reproductive capacity attenuation. Importantly, MMP significantly reversed the foregoing changes in NP-treated mice. Notably, it has been observed that the MMP therapy remarkably improved oxidative stress, apoptosis, autophagy and inflammatory responses, and suppressed the Akt/mTOR signaling pathway in testicular tissues. These results manifested that MMP might be a promising treatment strategy for ameliorating the biotoxicity of NP.

Physiological and transcriptional responses of Dictyosphaerium sp. under co-exposure of a typical microplastic and nonylphenol

Microplastics (MPs) and nonylphenol (NP) are typical pollutants that are frequently detected in aquatic environments and can pose a risk to aquatic organisms. However, the responses of algae, the producers in aquatic ecosystems, to MP and NP co-exposure have not been extensively investigated. In this study, polystyrene (PS, 50 mg/L) was selected as a representative MP to evaluate its short-term effects on algae treated with NP (4 mg/L). The results showed that PS mitigated the toxicity of NP to algae after 96 h of exposure, as illustrated by the higher cell densities and pigment concentrations, as well as lower extracellular protein contents and better integrity of intracellular structures, in algae subjected to PS + NP treatment compared with those subjected to NP treatment. Moreover, the upregulated expression of genes involved in photosynthesis and downregulated expression of ribosomal genes as well as genes encoding ATPase and antioxidase, analyzed through RNA-sequencing analysis, further indicated the potential repair and defense mechanisms of PS in NP-treated algae.

The antagonistic effect of bisphenol A and nonylphenol on liver and kidney injury in rats

Objective Bisphenol A (BPA) and nonylphenol (NP) are widely distributed endocrine-disrupting compounds. We aimed to estimate the combined toxicity of BPA and NP at a clinically safe dose (100 μg/kg) in rats. Materials and methods Liver and kidney functions were evaluated by detecting the relevant indicators. Hematoxylin and Eosin (HE) staining was performed to examine the injury in the tissue. TUNEL assay and Western blot were used to detect cell apoptosis and expressions of target factors, respectively. Results The body weight of rats in the BPA + NP group was lighter than that in the BPA or NP group. BPA or NP weakened liver function through increasing levels of aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine aminotransferase (ALT), cholesterol (CHOL), triglyceride TG, globulin (GLOB), treponemiapallidum (TP), and total bilirubin (TBIL). BPA and NP could induce kidney damage by elevating the levels of serum creatinine (Scr) and blood urea nitrogen (BUN). Moreover, the malondialdehyde (MDA) content was increased, whereas the activities of superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GSH-PX), glutathione sulfotransferase (GSH-ST), catalase (CAT), and peroxidase (POD) were reduced in those groups exposed to BPA or NP. HE staining exhibited injuries of the liver and kidney. Furthermore, the apoptosis of liver and kidney cells was enhanced by exposure to BPA or NP. Additionally, the expressions of CYP2D6, CYP1A1, and CYP2E1 were triggered by the treatment of BPA or NP. The combined effect of BPA and NP seemed to be antagonistic at a low dose. Conclusion BPA and NP may have potential interactions.

Nonylphenol exposure in Labeo rohita (Ham.): Evaluation of behavioural response, histological, haematological and enzymatic alterations

The impact of acute and chronic exposure of nonylphenol (NP) on behaviour, histopathology, haematology and biochemical parameters of Labeo rohita (Hamilton, 1822) was investigated in the current study. The 96 h LC50 of NP for L. rohita was estimated to be 0.548 mg L−1. Acute toxicity of NP induced several behavioural alternations. Further, sub-lethal NP exposure for a period of sixty days to 1/10th (0.0548 mg L−1), 1/15th (0.0365 mg L−1) and 1/20th (0.0274 mg L−1) of 96 h LC50 resulted a reduction in total erythrocyte count and haemoglobin content whereas the total leukocyte count was observed to increase significantly. Among the biochemical parameters, blood glucose level increased, but there was significant decrease in total serum protein, albumin and globulin level. Significant alterations occurred in the histological architecture of gill tissue in NP exposed groups. The catalase and superoxide dismutase activity in gill tissues were elevated significantly while the concentration dependent inhibition of acetylcholinesterase activity was observed on 20th, 40th and 60th day of NP exposure. An increased glutathione-S-transferase activity in gill tissue was also observed in NP exposed groups. The present ecotoxicological study provides a reliable indication for the obligation to control the use and safe disposal of NP.

Effects of Fe2O3 nanoparticles on extracellular polymeric substances and nonylphenol degradation in river sediment

In this study, the impact of Fe2O3 nanoparticles (nFe2O3) on microbial extracellular polymeric substances (EPS) and nonylphenol (NP) degradation in sediment were investigated. The results showed that the addition of nFe2O3 lowered the degree of EPS overproduction and the amount of polysaccharides and proteins secreted in NP contaminated sediment. Particularly, the secretion of colloidal EPS (C-EPS) lowered significantly (P < 0.05), and the content of tyrosine-like, tryptophan-like, and soluble microbial by-product-like substances in C-EPS also decreased, leading to a lower aromaticity, humification, and hydrophobicity of C-EPS. Furthermore, with lower C-EPS content in water, NP was adsorbed to sediment more easily, and the weakened toxic effect of NP to bacteria as well as a higher proportion of organic matter degrading microbes stimulated NP degradation. These findings revealed the vital role of nFe2O3 in alleviating NP toxicity to microbes and reducing NP ecological risk in aquatic environments.

Chemical- and species-specific toxicity of nonylphenol and octylphenol to microalgae Chlorella pyrenoidosa and Scenedesmus obliquus

As typical endocrine disrupters, nonylphenol (NP) and octylphenol (OP) are emerging pollutants that have attracted wide attention. This study investigated the toxicity effects of NP and OP on microalgae Chlorella pyrenoidosa and Scenedesmus obliquus, particularly on their growth inhibition, photosynthetic pigment, chlorophyll fluorescence, and superoxide dismutase and malondialdehyde levels. Results showed that the 96 h EC50 of NP and OP was 2.89 and 5.21 mg/L on C. pyrenoidosa, respectively, and 1.54 and 8.48 mg/L on S. obliquus, respectively. NP exerted a stronger inhibitory effect on cell growth, photosynthesis, and PSII activity, and it contributed more oxidative stress on C. pyrenoidosa than on S. obliquus. By contrast, OP exerted a stronger inhibitory effect on S. obliquus than on C. pyrenoidosa. Furthermore, the toxicity of OP to the tested microalgae was lower than that of NP. Principal component analysis (PCA) and Pearson’s correlation indicate that the accumulation of reactive oxygen species is the dominant mechanism of NP and OP cellular toxicity. The principal components of NP and OP affecting microalgae are distinct in the PCA plot, and different endocrine disrupters have varying chemical-specific influences on algal cells. This study confirmed that the toxicity of NP and OP to microalgae C. pyrenoidosa and S. obliquus is chemical- and species-specific. These findings should be considered when assessing the health risk of environmental pollution.

Nonylphenol exposure affects mouse oocyte quality by inducing spindle defects and mitochondria dysfunction

Nonylphenol (NP) is a chemical raw material and intermediate which is mainly used in the production of surfactants, lubricating oil additives and pesticide emulsifiers. NP is reported to be toxic on the immune system, nervous system and reproductive system due to its binding to estrogen receptors. However, the toxicity of NP on mammalian oocyte quality remains unclear. In present study, we explored the effects of NP exposure on mouse oocyte maturation. Our results showed that 4 weeks of NP exposure increased the number of atresia follicles and decreased oocyte developmental competence. Transcriptomic analysis indicated that NP exposure altered the expression of more than 800 genes in oocytes, including multiple biological pathways. Subcellular structure examination indicated that NP exposure disrupted meiotic spindle organization and caused chromosome misalignment. Moreover, aberrant mitochondrial distribution and decreased membrane potential were also observed, indicating that NP exposure caused mitochondria dysfunction. Further analysis showed that NP exposure resulted in the accumulation of reactive oxygen species (ROS), which causes oxidative stress; and the NP-exposed oocytes showed positive Annexin-V signal, indicating the occurrence of early apoptosis. In summary, our results indicated that NP exposure reduced oocyte quality by affecting cytoskeletal dynamics and mitochondrial function, which further induced oxidative stress and apoptosis in mice.

Reduced phytotoxicity of nonylphenol on tomato (Solanum lycopersicum L.) plants by earthworm casts

Concentrations as high as thousands of milligrams per kilogram (dry weight) of nonylphenol (NP), an endocrine-disrupting chemical of great concern, have been reported in soil. Soil is considered one of the primary pathways for exposure of crop plants to NP. However, there have been few studies on the toxicity of soil NP to crop plants, especially with comprehensive consideration of the application of organic fertiliser which is a common agricultural practice. In this study, tomato plants were grown in soils treated with NP in the presence and/or absence of earthworm casts (EWCs). After four weeks, we tested the physiological and biochemical responses (accumulative levels of hydrogen peroxide (H2O2) and superoxide anion radicals (O2-·), total chlorophyll content, degree of membrane lipid peroxidation, activities of defence-related enzymes, and level of DNA damage) and the changes in plant growth (elongation and biomass). The growth inhibition, reactive oxygen species (H2O2 and O2-·) accumulation, decrease in chlorophyll content, increase in activity of defence-related enzymes (including superoxide dismutase, peroxidase, catalase, ascorbate peroxidase, glutathione S-transferase and glutathione reductase), enhancement of membrane lipid peroxidation, and DNA damage in NP-treated seedlings were clearly reversed by the intervention of EWCs. In particular, the suppressed elongation, biomass, and chlorophyll content in tomato plants exposed to NP alone were significantly restored by EWCs to even greater levels than those of the undisturbed control. In other words, EWCs could efficiently invigorate the photosynthesis of crops via up-regulating the chlorophyll content, thereby overwhelming the NP stress on plant growth. Accordingly, except for reducing the bioavailability of soil NP as reported in our previous study, EWCs could also help crop plants to cope with NP stress by strengthening their stress resistance ability. Our findings are of practical significance for the formulation of strategies to relieve the negative effects of soil NP on crop growth.

Toxic Effects of Nonylphenol on Neonatal Testicular Development in Mouse Organ Culture.

Nonylphenol (NP) is an alkylphenol that is widely used in chemical manufacturing. Exposure to this toxic environmental contaminant has been shown to negatively affect the reproductive system. Herein, we evaluated the toxicity of NP in mouse testes, while using in vitro organ culture. Mouse testicular fragments (MTFs), derived from five-day postpartum neonatal mouse testes, were exposed to different concentrations of NP (1–50 μM) for 30 days. The results showed that NP impaired germ cell development and maintenance. Furthermore, NP significantly downregulated the transcript levels of both undifferentiated and differentiated germ cell marker genes relative to those in controls. In particular, a high dose of NP (50 µM) led to complete germ cell depletion and resulted in spermatogenic failure, despite the presence of Sertoli and Leydig cells. In addition, the mRNA expression of steroidogenic enzymes, such as steroidogenic acute regulatory protein (STAR), Cytochrome P450 Family 11 Subfamily A Member 1 (Cyp11α1), Cytochrome P450 17A1 (Cyp17α1), and androgen receptor (AR), increased with increasing concentration of NP. Conversely, the expression of estrogen receptor alpha (ESR1) and Cytochrome P450 family 19 subfamily A member 1 (Cyp19α1) in NP-exposed MTFs decreased when compared to that of the control. Taken together, this study demonstrates that NP has a negative effect on prepubertal spermatogenesis and germ cell maintenance and it disrupts steroidogenesis and induces hormonal imbalance in MTFs.

Enhanced excretion of extracellular polymeric substances associated with nonylphenol tolerance in Dictyosphaerium sp

Dictyosphaerium sp. is tolerant to nonylphenol (NP); however, knowledge regarding the mechanisms involved in NP tolerance is limited. In this study, a batch of algal culture experiments were carried out to elucidate the underlying mechanisms by investigating the production and composition of extracellular polymeric substances (EPS) in algae exposed to NP. The excretion of EPS was significantly enhanced (P < 0.001) in algae exposed to 4 and 8 mg/L of NP. The polysaccharides in soluble EPS and the proteins in bound EPS were specifically overproduced. The three-dimensional excitation and emission matrix fluorescence spectra analyses indicated that tyrosine- and tryptophan-like substances were the main functional compositions in the proteins of EPS. In addition, enhanced EPS secretion significantly alleviated the toxicity of NP to the algae by the reduction of cell internalization, as indicated by the higher IC50, biomass, and cell growth rate in the algae with EPS. These discoveries along with the characterizations by algal cell surface hydrophobicity analysis, scanning electron microscopy, and Fourier transform infrared spectra spectroscopy demonstrated the vital role of EPS in the algal resistance to NP.

The combined toxicity influence of microplastics and nonylphenol on microalgae Chlorella pyrenoidosa.

Microplastics and nonylphenol (NP) are considered as emerging pollutant and have attracted wide attention, while their combined toxicity on aquatic organisms is barely researched. Therefore, the combined toxicity influence of NP with three types of microplastics containing polyethylene (PE1000, 13μm and PE, 150μm), polyamide (PA1000, 13μm and PA, 150μm) polystyrene (PS, 150μm) on microalgae Chlorella pyrenoidosa was analyzed. Both growth inhibition, chlorophyll fluorescence, superoxide dismutase (SOD), malondialdehyde (MDA), and catalase (CAT) were determined. We found that single microplastics and NP both inhibited algal growth, thereby causing oxidative stress. The order of inhibition effect in single microplastics experiment was PE1000>PA1000>PE≈PS>PA. The combined toxicity experiment results indicated that the presence of microplastics had positive effect in terms of alleviating NP toxicity to C. pyrenoidosa, and the microplastics adsorption capacity to NP was the dominant contributing factor for this effect. According to the independent action model, the combined toxicity was antagonistic. Because the negative effect of smaller size microplastics on algal growth was aggravated with prolonged exposure time, the optimum effect of microplastics alleviated NP toxicity was PA1000 at 48h, while this effect was substituted by PA at 96h during combined toxicity. Thus, the toxicity of smaller size microplastics has a nonnegligible influence on combined toxicity. This study confirms that microplastics significantly affected the toxicity of organic pollutants on microalgae. Further research on the combined toxicity of smaller size microplastics with pollutants in chronic toxicity is needed.

Polysaccharide from the seeds of Plantago asiatica L. alleviates nonylphenol induced reproductive system injury of male rats via PI3K/Akt/mTOR pathway

• PLCP protected male rats against NP exposure induced reproductive system injury. • PLCP alleviated histopathologic injury in testis of NP induced rats. • PLCP relieved oxidative damage in testis and epididymis of NP induced rats. • PLCP ameliorated hormone expressions in serum and testis. • PLCP reduced NP-induced apoptosis and autophagy via PI3K/Akt/mTOR pathway. The preventive role of polysaccharide from the seeds of Plantago asiatica L. (PLCP) against reproductive system injury induced by nonylphenol (NP) was investigated. Male Sprague-Dawley rats were exposed orally to NP 1 h after PLCP intragastric administration continuously for 45 days. The results showed that NP induced significant decrease in relative weight of testes and epididymis, changed testicular histomorphology, and disrupted hormone secretions. Moreover, oxidative stress occurred after NP exposure by overproduction of Malondialdehyde, lipid peroxidation, inducible nitric oxide synthase, and low activities of superoxide dismutase and catalase. Furthermore, the induction of apoptosis and disturbance of PI3K/Akt/mTOR pathway by NP were also proved. Interestingly, PLCP alleviated NP toxicity by improving antioxidant enzymes, recovering hormone secretions, inhibiting apoptosis and autophagy, which involves PI3K/Akt/mTOR pathway. These findings provide a good direction that PLCP may be a good candidate to help body defend against toxic substance, particularly endocrine disrupting chemicals induced reproductive toxicity.

Toxicity of nonylphenol and nonylphenol ethoxylate on Caenorhabditis elegans

Among the most used chemicals in the world are nonionic surfactants. One of these environmental pollutants is nonylphenol ethoxylate (NP-9), also known as Tergitol, and its degradation product, nonylphenol (NP). The objective of this work was to determine the toxicity of NP and NP-9 in Caenorhabditis elegans. Wild-type L4 larvae were exposed to different concentrations of the surfactants to measure functional endpoints. Mutant strains were employed to promote the activation of toxicity signaling pathways related to mtl-2, gst-1, gpx-4, gpx-6, sod-4, hsp-70 and hsp-4. Additionally, stress response was also assessed using a daf-16::GFP transgenic strain. The lethality was concentration dependent, with 24-h LC50 of 122 μM and 3215 μM for NP and NP-9, respectively. Both compounds inhibited nematode growth, although NP was more potent; and at non-lethal concentrations, nematode locomotion was reduced. The increase in the expression of tested genes was significant at 10 μM for NP-9 and 0.001 μM for NP, implying a likely role for the activation of oxidative and cellular stress, as well as metabolism pathways. With the exception of glutathione peroxidase, which has a bimodal concentration-response curve for NP, typical of endocrine disruption, the other curves for this xenobiotic in the strains evaluated were almost flat for most concentrations, until reaching 50–100 μM, where the effect peaked. NP and NP-9 induced the activation and nuclear translocation of DAF-16, suggesting that transcription of stress-response genes may be mediated by the insulin/IGF-1 signaling pathway. In contrast, NP-9 induced a concentration-dependent response for the sod-4 and hsp-4 mutants, with greater fluorescence induction than NP at similar levels. In short, NP and NP-9 affect the physiology of C. elegans and modulate gene expression related to ROS production, cellular stress and metabolism of xenobiotics.

Bioaccumulation, growth performance, and transcriptomic response of Dictyosphaerium sp. after exposure to nonylphenol

Algal cultures of Dictyosphaerium sp. were treated with a wide range (0–8 mg/L) of nonylphenol (NP) applications to investigate the species' potential to perform bioremediation of NP-contaminated wastewater and explore the mechanism of NP toxicity in algal cell. The algal species exhibited a high tolerance for NP and efficiently removed even high concentrations of NP. The accumulation of NP in algal cells tended to increase and the percentage of NP adhered to the cell walls tended to decrease as the NP concentration increased. The thylakoid density and the pyrenoid size also tended to decrease as the NP concentration rose. The key genes involved in the antioxidative pathways and photosynthetic pathways were down-regulated in the NP-treated algal cells. Algal ribosome genes were especially sensitive to NP. The results indicated that NP could induce oxidative stress in algal cells and that Dictyosphaerium sp. showed potential as a bioremediation agent.