Impact of Mycotoxin Contaminations on Aquatic Organisms: Toxic Effect of Aflatoxin B1 and Fumonisin B1 Mixture

Paola, Davide Di; Iaria, Carmelo; Capparucci, Fabiano; Arangia, Alessia; Crupi, Rosalia; Cuzzocrea, Salvatore; Spanò, Nunziacarla; Gugliandolo, Enrico; Peritore, Alessio Filippo

doi:10.3390/toxins14080518

Cited by 22 publications

(8 citation statements)

References 54 publications

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“…After deparaffinization, endogenous peroxidase was quenched with 0.3% H 2 O 2 in 60% methanol for 30 min [ 83 ]. The sections were permeabilized with 0.1% Triton X-100 in phosphate-buffered saline (PBS) for 20 min [ 84 , 85 ]. Non-specific adsorption was minimized by incubating the section in 2% normal goat serum in phosphate-buffered saline for 20 min.…”

Section: Methodsmentioning

confidence: 99%

Chronic Exposure to Vinclozolin Induced Fibrosis, Mitochondrial Dysfunction, Oxidative Stress, and Apoptosis in Mice Kidney

Paola

D’Amico

Genovese

et al. 2022

IJMS

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Vinclozolin is one of the most used fungicides in the control of fungi in fruits, vegetables, and ornamental plants. The effects of its exposure on different organs have been described, but information regarding its relevance to vinclozolin-induced nephrotoxicity is largely missing. This study focuses on the potential mechanism of vinclozolin-induced nephrotoxicity. CD1 male mice were administered vinclozolin (100 mg/kg) by oral gavage for 28 days. Vinclozolin administration decreased body weight over the treatment period and at the end of the experiment, increased the ratio of kidney weight to body weight and increased serum urea nitrogen and creatinine contents. Vinclozolin also induced histopathological alterations, including tubular dilatation and necrosis and impaired the integrity of the renal-tubular architecture and kidney fibrosis. The analyses conducted showed that vinclozolin administration altered the mRNA levels of mitochondrial function-related proteins (SIRT3, SIRT1, PGC-1α, TFAM, NRF1, VDAC-1, and Cyt c) and oxidative stress (increased lipid peroxidation and decreased total antioxidative capacity, catalase, and superoxide dismutase activities, glutathione levels, and glutathione peroxidase activity) in the kidneys. Furthermore, vinclozolin induced toxicity that altered Nrf2 signalling and the related proteins (HO-1 and NQO-1). Vinclozolin administration also affected both the extrinsic and intrinsic apoptotic pathways, upregulating the expression of proapoptotic factors (Bax, Caspase 3, and FasL) and downregulating antiapoptotic factor (Bcl-2) levels. This study suggests that vinclozolin induced nephrotoxicity by disrupting the transcription of mitochondrial function-related factors, the Nrf2 signalling pathway, and the extrinsic and intrinsic apoptotic pathways.

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Section: Methodsmentioning

confidence: 99%

Chronic Exposure to Vinclozolin Induced Fibrosis, Mitochondrial Dysfunction, Oxidative Stress, and Apoptosis in Mice Kidney

Paola

D’Amico

Genovese

et al. 2022

IJMS

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“…At 72 and 96 hpf, the hatching rate was monitored to assess developmental delay. At 96 hpf, observations were performed to detect abnormalities, including pericardial edema, jaw development, yolk sac necrosis, swim bladder development, body axis shape/curvature, hemorrhage, and changes in pigmentation [ 95 ]. For imaging purposes, 96 hpf-old larvae were mounted in methylcellulose and photographed (Olympus SZ61, Olympus, Tokyo, Japan).…”

Section: Methodsmentioning

confidence: 99%

In Silico Analysis, Anticonvulsant Activity, and Toxicity Evaluation of Schisandrin B in Zebrafish Larvae and Mice

Nieoczym,

Banono,

Stępnik

et al. 2023

IJMS

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The aim of this study is to evaluate the anticonvulsant potential of schisandrin B, a main ingredient of Schisandra chinensis extracts. Schisandrin B showed anticonvulsant activity in the zebrafish larva pentylenetetrazole acute seizure assay but did not alter seizure thresholds in the intravenous pentylenetetrazole test in mice. Schisandrin B crosses the blood–brain barrier, which we confirmed in our in silico and in vivo analyses; however, the low level of its unbound fraction in the mouse brain tissue may explain the observed lack of anticonvulsant activity. Molecular docking revealed that the anticonvulsant activity of the compound in larval zebrafish might have been due to its binding to a benzodiazepine site within the GABAA receptor and/or the inhibition of the glutamate NMDA receptor. Although schisandrin B showed a beneficial anticonvulsant effect, toxicological studies revealed that it caused serious developmental impairment in zebrafish larvae, underscoring its teratogenic properties. Further detailed studies are needed to precisely identify the properties, pharmacological effects, and safety of schisandrin B.

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“…The following antibodies were used: anti-IkBα (1:1000, SCB, #sc1643), anti-NF-kB p65 (1:1000; SCB, #sc8414), anti-Nrf2 (1:5000; SCB, #sc365949), anti-HO-1 (1:5000; SCB, #sc136960), MnSOD (1:5000 SCB #sc137254), anti-β-actin (1:5000; SCB, #sc8432) and anti-lamin A/C antibody (1:5000; Sigma-Aldrich, St. Louis, MO, USA). The membranes were then incubated with IgG peroxidase-conjugated secondary antibody-conjugated bovine mouse IgG or IgG peroxidase-conjugated goat anti-rabbit (1:2000, Jackson ImmunoResearch, Baltimore, MD, USA) [ 58 , 62 , 63 , 64 ]. Protein expression was quantified by densitometry with BIORAD ChemiDocTM XRS + software and normalized to housekeeping genes β-actin and lamin A/C as previously reported [ 64 , 65 ].…”

Section: Methodsmentioning

confidence: 99%

Aerosol-Administered Adelmidrol Attenuates Lung Inflammation in a Murine Model of Acute Lung Injury

et al. 2022

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Acute lung injury (ALI) is a common and devastating clinical disorder with a high mortality rate and no specific therapy. The pathophysiology of ALI is characterized by increased alveolar/capillary permeability, lung inflammation, oxidative stress and structural damage to lung tissues, which can progress to acute respiratory distress syndrome (ARDS). Adelmidrol (ADM), an analogue of palmitoylethanolamide (PEA), is known for its anti-inflammatory and antioxidant functions, which are mainly due to down-modulating mast cells (MCs) and promoting endogenous antioxidant defense. The aim of this study is to evaluate the protective effects of ADM in a mice model of ALI, induced by intratracheal administration of lipopolysaccharide (LPS) at the dose of 5 mg/kg. ADM 2% was administered by aerosol 1 and 6 h after LPS instillation. In this study, we clearly demonstrated that ADM reduced lung damage and airway infiltration induced by LPS instillation. At the same time, ADM counteracted the increase in MC number and the expression of specific markers of MC activation, i.e., chymase and tryptase. Moreover, ADM reduced oxidative stress by upregulating antioxidant enzymes as well as modulating the Nf-kB pathway and the resulting pro-inflammatory cytokine release. These results suggest that ADM could be a potential candidate in the management of ALI.

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Impact of Mycotoxin Contaminations on Aquatic Organisms: Toxic Effect of Aflatoxin B1 and Fumonisin B1 Mixture

Cited by 22 publications

References 54 publications

Chronic Exposure to Vinclozolin Induced Fibrosis, Mitochondrial Dysfunction, Oxidative Stress, and Apoptosis in Mice Kidney

Chronic Exposure to Vinclozolin Induced Fibrosis, Mitochondrial Dysfunction, Oxidative Stress, and Apoptosis in Mice Kidney

In Silico Analysis, Anticonvulsant Activity, and Toxicity Evaluation of Schisandrin B in Zebrafish Larvae and Mice

Aerosol-Administered Adelmidrol Attenuates Lung Inflammation in a Murine Model of Acute Lung Injury

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