Mercury (Hg) and lead (Pb) are widespread contaminants that pose risks to avian scavengers. In fact, Pb exposure is the primary factor limiting population recovery in the endangered California condor (Gymnogyps californianus) and Hg can impair avian reproduction at environmentally relevant exposures. The Pacific Northwest region of the US was historically part of the condor's native range, and efforts are underway to expand recovery into this area. To identify potential threats to reintroduced condors we assessed foraging habitats, Hg and Pb exposure, and physiological responses in two surrogate avian scavenger species (common ravens [Corvus corax] and turkey vultures [Cathartes aura] across the region between 2012 and 2016. Mercury exposure near the Pacific coast was 17–27-fold higher than in inland areas, and stable carbon and sulfur isotopes ratios indicated that coastal scavengers were highly reliant on marine prey. In contrast, Pb concentrations were uniformly elevated across the region, with 18% of the birds exposed to subclinical poisoning levels. Elevated Pb concentrations were associated with lower delta-aminolevulinic acid dehydratase (δ-ALAD) activity, and in ravens there was an interactive effect between Hg and Pb on fecal corticosterone concentrations. This interaction indicated that the effects of Hg and Pb exposure on the stress axis are bidirectional, and depend on the magnitude of simultaneous exposure to the other contaminant. Our results suggest that condors released to the Pacific Northwest may be exposed to both elevated Hg and Pb, posing challenges to management of future condor populations in the Pacific Northwest. Developing a robust monitoring program for reintroduced condors and surrogate scavengers will help both better understand the drivers of exposure and predict the likelihood of impaired health. These findings provide a strong foundation for such an effort, providing resource managers with valuable information to help mitigate potential risks.

Methylisothiazolinone (MIT) has been widely used to control bacterial growth in reverse osmosis (RO) systems. However, MIT's toxicity on microalgae should be determined because residual MIT is concentrated into RO concentrate (ROC) and might have a severe impact on microalgae-based ROC treatment. This study investigated the tolerance of Scenedesmus sp. LX1 to MIT and revealed the mechanism of algal growth inhibition and toxicity resistance. Scenedesmus sp. LX1 was inhibited by MIT with a half-maximal effective concentration at 72 h (72 h-EC50) of 1.00 mg/L, but the strain recovered from the inhibition when its growth was not completely inhibited. It was observed that this inhibition's effect on subsequent growth was weak, and the removal of MIT was the primary reason for the recovery. Properly increasing the initial algal density significantly shortened the adaptation time for accelerated recovery in a MIT-containing culture. Photosynthesis damage by MIT was one of the primary reasons for growth inhibition, but microalgal cell respiration and adenosine triphosphate (ATP) synthesis were not completely inhibited, and the algae were still alive even when growth was completely inhibited, which was notably different from observations made with bacteria and fungi. The algae synthesized more chlorophyll, antioxidant enzymes of superoxide dismutase (SOD) and catalase (CAT), and small molecules, such as reduced glutathione (GSH), to resist MIT poisoning. The microalgae-based process could treat the MIT-containing ROC, since MIT was added for only several hours a week in municipal wastewater reclamation RO processes, and the MIT average concentration was considerably lower than the maximum concentration that algae could tolerate.

Large amounts of aluminum (Al) are found in wastewater from industrial bauxite mining, which is often responsible for the contamination of drinking water sources in urban and rural communities. Although this metal exhibits broad environmental distribution, its cardiac repercussions are poorly understood, making it difficult to establish diagnostic criteria in cases of Al intoxication. In the absence of clinical data, we used a preclinical model to investigate the impact of Al exposure on heart bioaccumulation, molecular oxidation, micromineral distribution, structural and ultrastructural remodeling of the cardiac tissue. Male Wistar rats were equally randomized into five groups: G1 = distilled water; and G2 to G5 = 0.02, 0.1, 50, and 200 mg/kg aluminum solution, respectively. After 120 days, the hearts were collected and subjected to mineral microanalysis, immunoenzymatic detection of 8-OHdG, as well as bright field, polarizing, scanning and transmission electron microscopy to estimate the extent of the cardiac remodeling and cardiomyocytes ultrastructure. Long-term Al exposure induced dose-dependent bioaccumulation, micromineral imbalance, genomic DNA oxidation, structural and ultrastructural abnormalities of the cardiac tissue, resulting in extensive parenchymal loss, stromal expansion, diffuse inflammatory infiltrate, increased glycoconjugate and collagen deposition, subversion and collapse of the collagen network, reduced myocardial vascularization index, mitochondrial swelling, sarcomere disorganization, myofilament dissociation, and fragmentation in cardiomyocytes. Our findings indicated that the heart was sensitive to Al-mediated toxicity, especially in animals treated with the three highest doses of Al. In response to Al-induced loss of the parenchyma, heart stroma exhibited a reactive and compensatory expansion, which, in combination with the increased distribution of thick myofibrils and degenerated mitochondria in cardiomyocytes, provides morphological evidence that cardiac tissue adaptations are not enough to adjust the relationships between the parenchyma and stroma until a steady state is reached, resulting in continuous pathological remodeling potentially associated with Al-induced proinflammatory and pro-oxidant events.

In the current study, the possible prophylactic and therapeutic effects of colostrum (COL) on acute organ injury caused by paracetamol (PAR) in rats were evaluated. Within the scope of this study, a 2-month-old male (150–200 g) 70 Wistar Albino rat was used and a total of seven groups were designed. The first group (CNT) was maintained for control purposes. The second group (COL-1) was given COL for 1 day, at a dose of 500 mg/kg at 6-h intervals, and blood and tissue sampling was performed at 24 h. The third group (COL-7) received COL for 7 days, at a dose of 500 mg/kg at 6-h intervals on day 1 and at a daily dose of 500 mg/kg on the following days, and blood and tissue samples were taken at the end of seventh day. The fourth group (PAR-1) was administered with PAR at a dose of 1.0 g/kg bw and was blood and tissue sampled at 24 h. The fifth group (PAR-7) received PAR at a dose of 1.0 g/kg bw on day 1 and was blood and tissue was removed at the end of day 7. The sixth group (PAR+COL-1) was administered with a combination of PAR (1 g/kg bw) and COL (500 mg/kg at 6-h intervals), and blood and tissue samples were collected at 24 h. The seventh group (PAR+COL-7) received 1.0 g/kg bw of PAR on day 1 and was given COL throughout the 7-day study period (at a dose of 500 mg/kg at 6-h intervals on day 1 and at a daily dose of 500 mg/kg on the following days). In the seventh group, blood and tissue samples were taken at the end of seventh day. Alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), glucose, creatinine, triglyceride, total bilirubin, total protein and albumin levels/activities were analysed in the serum samples. The malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) levels/activities, known as oxidative stress parameters, were assayed for tissue homogenates and blood (erythrocytes/plasma); in addition, enzyme activities of GSH S-transferase (GST), cytochrome P4502E1 (CYP2E1), NADH-cytochrome b5 reductase (CYTB5), glucose-6-phosphate dehydrogenase (G6PD), NADPH-cytochrome P450 C reductase (CYTC) and glutathione (GSH) levels/activities defined as drug metabolising parameters were measured in liver homogenates. In result, it was determined that PAR caused significant alterations in some biochemical and lipid peroxidation parameters and the activities/levels of drug metabolising parameters in the liver and that COL normalised some of these parameters and reduced PAR-induced tissue damage.

The kidney is one of the main organs affected by lead toxicity. We investigated the effects of berberine on lead-induced nephrotoxicity in adult male Wistar rats. Animals received an aqueous solution of lead acetate (500 mg Pb/L in the drinking water) and/or berberine (50 mg/kg, i.g.) for 8 weeks. Lead caused an increase in malondialdehyde (P < 0.001) and total oxidant status (P < 0.01), and a decrease in reduced glutathione (P < 0.001), catalase (P < 0.01), superoxide dismutase (P < 0.001), and total antioxidant capacity (P < 0.05). Berberine prevented the prooxidant and antioxidant imbalance induced by lead (P < 0.001). Berberine corrected the increased relative kidney weight (P < 0.05) and biomarkers of renal function (creatinine (P < 0.001), urea (P < 0.05), uric acid (P < 0.001), albumin (P < 0.01), and total protein (P < 0.05)) in lead group. It also attenuated lead-induced abnormal renal structure. The results confirmed renoprotective effects of berberine in an animal model of lead-induced nephrotoxicity by molecular, biochemical, and histopathological analysis through inhibiting lipid peroxidation and enhancing antioxidant defense system mechanisms. Therefore, berberine makes a good candidate to protect against the deleterious effect of chronic lead intoxication.

Many environmental agents, such as excessive alcohol intake, xenobiotics, and virus, are able to damage the human body, targeting especially the liver. Metal excess may also assault the liver. Thus, chronic iron overload may cause, especially when associated with cofactors, diffuse organ damage that is a source of significant morbidity and mortality. Iron excess can be either of acquired (mostly transfusional) or of genetic origin. Hemochromatosis is the archetype of genetic iron overload diseases and represents a serious health problem. A better understanding of iron metabolism has deeply modified the hemochromatosis field which today benefits from much more efficient diagnostic and therapeutic approaches.

As cofactors of several enzymatic, copper (Cu) participates in many essential metabolic processes. Also, as a heavy metal, it exhibits highly toxic to the organism if excessive. This study endeavored to detect the pathophysiological changes in the jejunum of chickens, which were insulted by CuSO₄ (300 mg/kg diet) for 90 days. Results showed metabolic disorders of trace elements evidenced by their significant downregulations (Na, Al, Li, B, Cr, Ni, Sn, Sb, Ba) and upregulations (Cu, Si, As, Cd, Se, and Tl) in 90 days. Simultaneously, increased TdT-mediated dUTP nick end labeling (TUNEL)-positive nuclei and distinct ultrastructural apoptotic features were observed. Meanwhile, in 30, 60, and 90 days, indicators of oxidative stress, apoptosis, autophagy, and mitochondrial dynamic were detected to uncover the molecular mechanism behind these pathological changes. The results showed that suppressed antioxidant ability was companied by increased mRNA and protein levels of proapoptosis and mitochondrial fission activating genes in the Cu group compared with chickens in the control group (P < 0.05). Moreover, the markers of autophagy long-chain 3 (LC3-II/LC3-I), Bcl-2-interacting protein (beclin-1), and autophagy-related gene (ATG4B and ATG5) displayed a time-dependent increase during 30, 60, and 90 days. We conjectured that subchronic copper poisoning, under the background of redistribution of trace elements, induced oxidative stress and cascaded apoptosis, autophagy, and mitochondrial disorder, which contributed to jejunotoxicity in chicken. Collectively, our study provides a basic assessment of subchronic Cu exposure on poultry, voicing concerns about copper pollution by anthropogenic activities.

Cd is a hazardous substance and carcinogen that is present in the environment; it is known to cause toxic effects in living organisms. Sulforaphane is a naturally available phytochemical with antioxidant, anti-inflammatory, and anticarcinogenic properties. However, the effects of sulforaphane on Cd toxicity in human mesenchymal stem cells (hMSCs) are unknown. In the present study, we investigated the molecular mechanisms of the effects of sulforaphane on Cd toxicity in hMSCs by using MTT assays, acridine orange/ethidium bromide staining, Hoechst staining, LysoRed staining, assessment of mitochondrial membrane potential, and gene expression analysis. Cd decreased hMSC viability in a dose-dependent manner with an IC₅₀ value of 56.5 μM. However, sulforaphane did not induce any significant reduction in cell viability. Nuclear morphological analysis revealed that Cd induced necrotic cell death. Additionally, Cd caused mitochondrial membrane potential loss in hMSCs. The treatment of Cd-exposed cells with sulforaphane (Cd-sulforaphane co-treatment) resulted in a significant recovery of the cell viability and nuclear morphological changes compared with that of cells treated with Cd only. The gene expression pattern of cells co-treated with Cd-sulforaphane was markedly different from that of Cd-treated cells, owing to the reduction in Cd toxicity. Our results clearly indicated that sulforaphane reduced Cd-induced toxic effects in hMSCs. Overall, the results of our study suggested that sulforaphane-rich vegetables and fruits can help to improve human health through amelioration of the molecular effects of Cd poisoning.

The aim of this study is to investigate the effects of arsenic (As) and copper (Cu) on the inflammatory response, and the protective roles of heat shock proteins (Hsps) in chicken testes. Seventy-two 1-day-old male Hy-line chickens were treated with 30 mg/kg feed of arsenic trioxide (As₂O₃) and/or 300 mg/kg feed of copper sulfate (CuSO₄) for 4, 8, and 12 weeks. The histological changes, inducible nitric oxide synthase (iNOS) activity, and the expressions of Hsps and inflammatory cytokines were detected. The results showed that slight histology changes were obvious in the testis tissue exposure to treatment groups. The activity and the protein level of iNOS were increased compared to the control group. The mRNA levels of proinflammatory cytokines and inflammatory factors were increased as a whole. However, anti-inflammatory cytokines were inhibited. The mRNA and protein levels of Hsp60, Hsp70, and Hsp90 were upregulated. These results suggested that sub-chronic exposure to As and/or Cu induced testicular poisoning in chickens. Increased Hsps tried to protect chicken testis tissues from tissues damage caused by inflammation. In conclusion, testicular poisoning induced by As and/or Cu caused inflammatory response and heat shock protein response in chicken testis tissues.

Chromium (Cr) is one of the most important environmental pollutants which are released into the environment due to their wide usage in numerous industries. The excess of Cr (VI) can induce hepatotoxicity, while the molecular mechanism that is involved in Cr (VI)-induced hepatotoxicity is unclear. We demonstrated the induction of chromium poisoning model in chickens to identify the differentially expressed genes (DEGs), and their functions were analyzed under different physiological and pathological conditions. Histopathological examination and transcriptome data for chromium-poisoned livers and control livers were annotated with Illumina® HiSeq 2000. The histopathological examination in chromium poisoning groups showed diapedesis, hemolysis, degeneration, nucleus pycnosis, and central phlebectasia in the liver. A total of 334 genes were upregulated and 509 genes were downregulated. The most strongly upregulated genes were HKDC1, DDX4, ACACA, FDFT1, CYYR1, PPP1R3C, and SLC16A14, while the most downregulated genes were MYBPC3, CCKAR, PCK1, and CPT1A. A Gene Ontology (GO) term with the highest enrichment of DEGs is small molecule metabolic process. In cell component domain, the term with the highest enrichment is extracellular matrix. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways showed that glucose metabolism, lipid metabolism, and protein metabolism were the most important metabolic pathways in the liver. The current study first time provides important clues and evidence for identifying the differentially expressed genes in livers due to Cr (VI)-induced liver injury in chickens.