Per- and Poly-fluoroalkyl substances (PFAS) are one of the major persistent environmental contaminants. Epidemiological studies have linked PFAS exposures to altered immunity and increased occurrence of infections in children. However, the mechanisms leading to immune susceptibility to bacterial infections remains unclear. To elucidate the mechanism, transcriptional alteration in the Caenorhabditis elegans model caused by a PFAS contaminated environmental water and two reconstituted PFAS solutions were evaluated using RNA-sequencing. PFAS affected the expression of several genes involved in C. elegans immune surveillance to Gram-positive bacteria (cpr-2, tag-38, spp-1, spp-5, clec-7, clec-172). The combined exposure to PFAS and Staphylococcus aureus significantly reduced C. elegans survival and increased intestinal membrane permeability. Furthermore, the growth of S. aureus in the presence of PFAS increased the expression of virulence genes, specifically, the virulence gene regulator saeR and α-hemolysin, hla, which resulted in increased hemolytic activity. The present study demonstrated that PFAS exposure not only increased C. elegans susceptibility to pathogens by reducing host immunity and increasing intestinal membrane permeability, but also increased bacteria virulence. This presents a broader implication for humans and other animals, where environmental contaminants simultaneously reduce host resilience, while, increasing microbial pathogenicity.

As part of a field campaign that studied the impact of Mexico City pollution plume at the local, sub-regional and regional levels, we studied transport-related changes in PM₁₀ composition, oxidative potential and in vitro toxicological patterns (hemolysis, DNA degradation). We collected PM₁₀ in Mexico City (T₀) and at a suburban-receptor site (T₁), pooled according to two observed ventilation patterns (T₀ → T₁ influence and non-influence). T₀ samples contained more Cu, Zn, and carbon whereas; T₁ samples contained more of Al, Si, P, S, and K (p < 0.05). Only SO₄ ⁻² increased in T₁ during the influence periods. Oxidative potential correlated with Cu/Zn content (r = 0.74; p < 0.05) but not with biological effects. T₁ PM₁₀ induced greater hemolysis and T₀ PM₁₀ induced greater DNA degradation. Influence/non-influence did not affect oxidative potential nor biological effects. Results indicate that ventilation patterns had little effect on intrinsic PM₁₀ composition and toxicological potential, which suggests a significant involvement of local sources.

The dinoflagellate Karlodinium veneficum has worldwide distribution and is associated with harmful algal blooms through the production of karlotoxins. We investigated the allelopathy and toxicity to explore the potential ecological implications. Prorocentrum donghaiense was inhibited significantly when grown either in co-cultures or in culture filtrate of K. veneficum. In addition, the effect of the co-occurring microalga species (P. donghaiense) on the hemolytic activity of K. veneficum was also evaluated. P. donghaiense did not inhibit the growth of K. veneficum but increased the hemolytic activity. The culture of K. veneficum was loaded onto an RP-C18 column and eluted with different percentages of aqueous methanol solution. 80% methanol fraction not only inhibited the growth of P. donghaiense by allelopathy but also exhibited strong hemolytic activity, indicating that the allelochemicals and toxins of K. veneficum might be the same components. Furthermore, KmTx 3 (C₆₈H₁₂₄O₂₄) was identified using HPLC-HRMS from this fraction.

Biosurfactants are surface active materials that are produced by some microorganisms. These molecules increase biodegradation of insoluble pollutants. In this study sediments and seawater samples were collected from the coastline of Bushehr provenance in the Persian Gulf and their biosurfactant producing bacteria were isolated. Biosurfactant producing bacteria were isolated by using an enrichment method in Bushnell-Hass medium with diesel oil as the sole carbon source. Five screening tests were used for selection of Biosurfactant producing bacteria: hemolysis in blood agar, oil spreading, drop collapse, emulsification activity and Bacterial Adhesion to Hydrocarbon test (BATH). These bacteria were identified using biochemical and molecular methods. Eighty different colonies were isolated from the collected samples. The most biosurfactant producing isolates related to petrochemical plants of Khark Island. Fourteen biosurfactant producing bacteria were selected between these isolates and 7 isolates were screened as these were predominant producers that belong to Shewanella alga, Shewanella upenei, Vibrio furnissii, Gallaecimonas pentaromativorans, Brevibacterium epidermidis, Psychrobacter namhaensis and Pseudomonas fluorescens. The largest clear zone diameters in oil spreading were observed for G. pentaromativorans strain O15. Also, this strain has the best emulsification activity and reduction of surface tension, suggesting it is the best of thee isolated strains. The results of this study confirmed that there is high diversity of biosurfactant producing bacteria in marine ecosystem of Iran and by application of these bacteria in petrochemical waste water environmental problems can be assisted.

Benthic dinoflagellates produce a diverse range of phycotoxins, which are responsible for intoxication events in marine fauna. This study assessed the hemolysis associated toxicities of six species of benthic dinoflagellates from the genera Coolia, Fukuyoa, Amphidinium and Prorocentrum. Results demonstrated that Amphidinium carterae, Coolia tropicalis and Fukuyoa ruetzleri were the three most toxic species, while Prorocentrum cf. lima did not have significant hemolytic effect. Grouper samples (Cephalopholis boenak) were more tolerant to the hemolytic algae than the blackhead seabream (Acanthopagrus schlegelii), with decreased heart rate and blood flow being observed in medaka larvae after exposure to toxic algal extracts. LC-MS/MS analysis detected a gambierone analogue called 44-methylgambierone produced by the C. tropicalis isolate. This analogue was also detected in the F. ruetzleri isolate. This study provided new information on the hemolysis associated toxicities of local toxic benthic dinoflagellates, which contributes to better understanding of their emerging threats to marine fauna and reef systems in Hong Kong.

Preservative treatments increase the durability of wood, and one of the alternative treatments involves the use of chromated copper arsenate (CCA). Due to the toxicity of CCA, the disposal of CCA-treated wood residues is problematic, and burning is considered to provide a solution. The ecotoxicological potential of ash can be high when these components are toxic and mutagenic. The aim of this study was to evaluate the toxicity and genotoxicity of bottom ash leachates originating from CCA-treated wood burning. Physical-chemical analysis of the leachates revealed that in treated wood ashes leachate (CCA-TWBAL), the contents of arsenic and chromium were 59.45 mg.L⁻¹ and 54.28 mg.L⁻¹, respectively. In untreated wood ashes leachate (UWBAL), these contents were 0.70 mg.L⁻¹ and 0.30 mg.L⁻¹, respectively. CCA-TWBAL caused significant toxicity in Lactuca sativa, Allium cepa, and microcrustacean Artemia spp. (LC50 = 12.12 mg.mL⁻¹). Comet assay analyses using NIH3T3 cells revealed that concentrations ranging from 1.0 and 2.5 mg.mL⁻¹ increase the damage frequency (DF) and damage index (DI). According to MTT assay results, CCA-TWBAL at concentrations as low as 1 mg.mL⁻¹ caused a significant decrease in cellular viability. Hemolysis assay analyses suggest that the arsenic and chromium leachate contents are important for the ecotoxic, cytotoxic, and genotoxic effects of CCA-TWBAL.

Copper (Cu) is one of the toxic elements that cause environmental pollution. As a result of excessive accumulation of copper in the organism, it causes damage in various organs and tissues and hemolysis in erythrocytes. Astaxanthin (ATX) is a pigment belonging to the xanthophyll family, which is an oxygenated derivative of carotenoids. Thanks to its powerful antioxidant properties, ATX has an extraordinary potential to protect the organism against various diseases, especially cancer. The main objective of this study was to investigate the toxic effect of copper ions on the glucose 6-phosphate dehydrogenase (G6PD), 6-phospho-gluconate dehydrogenase (6PGD), glutathione reductase (GR), glutathione S-transferase (GST), and thioredoxin reductase (TrxR) enzymes and the role of astaxanthin in reducing this effect. In in vivo study, Wistar Albino male rats (n=28) were randomly divided into 4 groups: the control group, copper (Cu2+) group, astaxanthin (ATX) group, and copper + astaxanthin (Cu2++ATX) group. The results show that G6PD enzyme activity in Cu2+ group was strongly inhibited (p ˂ 0.05), while in other groups, there were no significant effects compared to the control group (p ⩾ 0.05). 6PGD enzyme activity was significantly reduced in Cu2+ group compared to that in the control group (p ˂ 0.05), and GR enzyme activity was lower in Cu2+ group compared to that in the control group (p ˂ 0.05). Similarly, when GST enzyme activity was evaluated, a strong decrease was observed in the Cu2+ group compared to that in the control group (p ˂ 0.05), while the enzyme activity in the Cu2++ATX group approached the control group (p ⩾ 0.05). When TrxR enzyme activity level was examined, a statistically significant decrease was observed in the Cu2+ and Cu2++ATX groups (p ˂ 0.05), and the enzyme activity in the ATX group was found to be close to that in the control group. When in vitro results were evaluated, it was observed that copper ions inhibited G6PD enzyme purified from rat erythrocyte tissues with IC50=1.90 μM value and Ki = 0.97 μM ± 0.082 value and the inhibition was non-competitive. From the results, it can be concluded that Cu2+ ions have an inhibitory effect on rat erythrocyte pentose phosphate pathway and antioxidant system enzymes both in vivo and in vitro, and astaxanthin reduces this effect.

Dermaseptins are peptides found in the skin secretions of Phyllomedusinae frogs. These peptides exert a lytic action on various microorganisms and have no considerable hemolytic effect except dermaseptin S4 (DS4) which exhibits a powerful cytotoxic effect. Therefore, we synthesized several analogs of DS4 in an attempt to find molecules with a weak hemolytic effect and significant bioactivities. In this study, we performed the synthesis of truncated peptides by introducing C-terminal and N-terminal amino acid deletions of the native sequence. All peptide analogs, in comparison with parental peptide, were tested firstly on human red blood cells to work out their cytotoxicity, secondly on the multidrug-resistant bacteria by trying to find MICs, and finally on colon cancer tumor cell line SW620 using the MTT test so as to investigate the anti-proliferative effect. Our results showed that, on the one hand, the N terminus of the native peptide was necessary for the antibacterial activity and the anti-proliferative effect of the peptide. On the other hand, the hemolytic activity was more notable in the sequences broken down on the C-terminal side.

The present study was designed to evaluate in vitro and in vivo the potential anti-inflammatory and nephroprotective potential of ethyl acetate fraction extracted from Fumaria officinalis (EAF) against permethrin (PER). Male wistar rats were treated daily by gavage during 7 days as follows: group C: negative control rats received 2 mL/kg bw of corn oil, group EAF: positive control rats received EAF at a dose of 200 mg/kg bw dissolved in water, group PER: rats received PER at a dose of 34.05 mg/kg bw and group (PER + EAF): rats received PER (34.05 mg/kg bw) and EAF (200 mg/kg bw). In vitro study showed the ability of EAF to inhibit protein denaturation and heat-induced hemolysis confirming its anti-inflammatory activity. In vivo, PER treatment decreased calcium (Ca) and phosphorus (P) levels and increased lactate dehydrogenase (LDH) activity in plasma. It induced oxidative stress objectified by an increase in the lipid peroxidation and protein oxidation and a perturbation of antioxidant system in kidney and mitochondria. The activities of NADH–ubiquinone reductase, ubiquinol–cytochrome C reductase and cytochrome C oxidase activities were reduced. These alterations were confirmed by histopathological studies. Co-treatment with EAF improved the antioxidant status and mitochondrial bioenergetics. The nephroprotective effects of EAF could be attributed to its modulation of detoxification enzymes and/or free radical scavenging actions.

p-Nitrophenol (PNP) is the main end product of organophosphorus insecticides and a derivative of diesel exhaust particles. In addition to its unfavorable impact on reproductive functions in both genders, it also has various harmful physiological effects including lung cancer and allergic rhinitis. The identification of the cellular readout that functions in metabolic pathway perpetuation is still far from clear. This research aimed to study the impact of chronic PNP exposure on the health condition of the liver in Japanese quails. Quails were exposed to different concentrations of PNP as follows: 0.0 (control), 0.01mg (PNP/0.01), 0.1mg (PNP/0.1), and 1mg (PNP/1) per kg of body weight for 2.5 months through oral administration. Liver and plasma samples were collected at 1.5, 2, and 2.5 months post-treatment for biochemical, histopathology, and immunohistochemistry assessment. The plasma aspartate aminotransferase (AST) level was assessed enzymatically. The livers were collected for histopathology, glycogen accumulation, proliferating cell nuclear antigen (PCNA), and apoptosis assessment. Our results revealed an irregularity in body weight due to the long-term exposure of PNP with a significant reduction in liver weight. PNP treatment caused histopathological alterations in the hepatic tissues which increased in severity by the long-term exposure. The low dose led to mild degeneration with lymphocytic infiltration, while the moderate dose has a congestion effect with some necrosis; meanwhile severe hepatocyte degeneration and RBCs hemolysis were noticed due to high dose of PNP. Glycogen accumulation increased in hepatocytes by prolonged exposure to p-Nitrophenol with the highest intensity in the group treated by the high dose. Moderate and high doses of PNP resulted in a significant increase in apoptosis and hepatocytes’ proliferation at the different time points after treatment. This increase is markedly notable and maximized at 2.5 months post-treatment. The damage occurred in a time-dependent manner. These changes reflected on the plasma hepatic enzyme AST that was clearly increased at 2.5 months of exposure. Therefore, it could be concluded that PNP has profound toxic effects on the liver in cellular level. Taking into consideration the time and dose factors, both have a synergistic effect on the accumulation of glycogen, apoptosis, and cellular proliferation, highlighting the power of cellular investigation which will potentially open the door for earlier medical intervention to counteract this toxicity. Collectively, PNP could have critical hurtful effects on the health of human beings, wild animals as well as livestock.