Review on the hazardous applications and photodegradation mechanisms of chlorophenols over different photocatalysts

The comet assay has become one of the methods of choice for the evaluation and measurement of DNA damage. It is sensitive, quick to perform and relatively affordable for the evaluation of DNA damage and repair at the level of individual cells. The comet assay can be applied to virtually any cell type derived from different organs and tissues. Even though the comet assay is predominantly used on human cells, the application of the assay for the evaluation of DNA damage in yeast, plant and animal cells is also quite high, especially in terms of biomonitoring. The present extensive overview on the usage of the comet assay in animal models will cover both terrestrial and water environments. The first part of the review was focused on studies describing the comet assay applied in invertebrates. The second part of the review, (Part 2) will discuss the application of the comet assay in vertebrates covering cyclostomata, fishes, amphibians, reptiles, birds and mammals, in addition to chordates that are regarded as a transitional form towards vertebrates. Besides numerous vertebrate species, the assay is also performed on a range of cells, which includes blood, liver, kidney, brain, gill, bone marrow and sperm cells. These cells are readily used for the evaluation of a wide spectrum of genotoxic agents both in vitro and in vivo. Moreover, the use of vertebrate models and their role in environmental biomonitoring will also be discussed as well as the comparison of the use of the comet assay in vertebrate and human models in line with ethical principles. Although the comet assay in vertebrates is most commonly used in laboratory animals such as mice, rats and lately zebrafish, this paper will only briefly review its use regarding laboratory animal models and rather give special emphasis to the increasing usage of the assay in domestic and wildlife animals as well as in various ecotoxicological studies.

/pdf/the-comet-assay-in-animal-models-from-bugs-to-whales-part-1-49pm4pf0k4.pdf

The comet assay in animal models: From bugs to whales - (Part 1 Invertebrates).

Zebrafish as the toxicant screening model: Transgenic and omics approaches.

Influence of multi-walled carbon nanotubes on the microbial biomass, enzyme activity, and bacterial community structure in 2,4-dichlorophenol-contaminated sediment

Experimental liver injury with hepatocelluar necrosis and abnormal liver tests is caused by exposure to heavy metals (HMs) like aluminum, arsenic, beryllium, cadmium, chromium, cobalt, copper, iron, lead, mercury, molybdenum, nickel, platinum, thallium, titanium, vanadium, and zinc. As pollutants, HMs disturb the ecosystem, and as these substances are toxic, they may affect the health of humans and animals. HMs are not biodegradable and may be deposited preferentially in the liver. The use of animal models can help identify molecular and mechanistic steps leading to the injury. HMs commonly initiate hepatocellular overproduction of ROS (reactive oxygen species) due to oxidative stress, resulting in covalent binding of radicals to macromolecular proteins or lipids existing in membranes of subcellular organelles. Liver injury is facilitated by iron via the Fenton reaction, providing ROS, and is triggered if protective antioxidant systems are exhausted. Ferroptosis syn pyroptosis was recently introduced as mechanistic concept in explanations of nickel (Ni) liver injury. NiCl2 causes increased iron deposition in the liver, upregulation of cyclooxygenase 2 (COX-2) protein and mRNA expression levels, downregulation of glutathione eroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1), nuclear receptor coactivator 4 (NCOA4) protein, and mRNA expression levels. Nickel may cause hepatic injury through mitochondrial damage and ferroptosis, defined as mechanism of iron-dependent cell death, similar to glutamate-induced excitotoxicity but likely distinct from apoptosis, necrosis, and autophagy. Under discussion were additional mechanistic concepts of hepatocellular uptake and biliary excretion of mercury in exposed animals. For instance, the organic anion transporter 3 (Oat3) and the multidrug resistance-associated protein 2 (Mrp2) were involved in the hepatic handling of mercury. Mercury treatment modified the expression of Mrp2 and Oat3 as assessed by immunoblotting, partially explaining its impaired biliary excretion. Concomitantly, a decrease in Oat3 abundance in the hepatocyte plasma membranes was observed that limits the hepatic uptake of mercury ions. Most importantly and shown for the first time in liver injury caused by HMs, titanium changed the diversity of gut microbiota and modified their metabolic functions, leading to increased generation of lipopolysaccharides (LPS). As endotoxins, LPS may trigger and perpetuate the liver injury at the level of gut-liver. In sum, mechanistic and molecular steps of experimental liver injury due to HM administration are complex, with ROS as the key promotional compound. However, additional concepts such as iron used in the Fenton reaction, ferroptosis, modification of transporter systems, and endotoxins derived from diversity of intestinal bacteria at the gut-liver level merit further consideration.

https://www.mdpi.com/1422-0067/23/20/12213/pdf?version=1666060982

Aluminum, Arsenic, Beryllium, Cadmium, Chromium, Cobalt, Copper, Iron, Lead, Mercury, Molybdenum, Nickel, Platinum, Thallium, Titanium, Vanadium, and Zinc: Molecular Aspects in Experimental Liver Injury

2,4-Dichlorophenol induces feminization of zebrafish (Danio rerio) via DNA methylation

2,4-Dichlorophenol induced feminization of zebrafish by down-regulating male-related genes through DNA methylation.

Effects of 2,4-dichlorophenol exposure on zebrafish: Implications for the sex hormone synthesis

Thallium(I and III) exposure leads to liver damage and disorders of fatty acid metabolism in mice.

2,4-Dichlorophenol (2,4-DCP) is one of the most abundant chlorophenols in the aquatic environment and has been frequently detected in surface waters. Although ecological and cellular toxicity of 2,4-DCP has aroused the public concern, few reports focus on the genotoxicity, especially on DNA double strand breaks (DSBs), of 2,4-DCP in fish. The present study aims to explore the genotoxic effect of 2,4-DCP on DSBs in goldfish Carassius auratus and to further elucidate its potential mechanism. The results showed that 2,4-DCP significantly induced DSBs (detected by neutral comet assay) in erythrocytes and hepatocytes of goldfish in a dose-dependent manner, indicating a genotoxicity of 2,4-DCP on fish. The total antioxidant capability and the content of reduced glutathione (GSH) were significantly decreased, while the level of reactive oxygen species (ROS) was significantly increased in a dose-dependent manner in erythrocytes and hepatocytes, suggesting an oxidative stress caused by 2,4-DCP in fish. N-acetyl-l-cysteine, a precursor of GSH and a ROS scavenger, significantly impaired 2,4-DCP-induced ROS overproduction and DSBs, which proves that ROS accumulation and GSH depletion are involved in 2,4-DCP-induced DNA damage in fish. Environ. Mol. Mutagen. 59:798-9, 2018. © 2018 Wiley Periodicals, Inc.

Dong Li

Papers

2,4-Dichlorophenol induces feminization of zebrafish (Danio rerio) via DNA methylation

2,4-Dichlorophenol induced feminization of zebrafish by down-regulating male-related genes through DNA methylation.

Effects of 2,4-dichlorophenol exposure on zebrafish: Implications for the sex hormone synthesis

Thallium(I and III) exposure leads to liver damage and disorders of fatty acid metabolism in mice.

2,4-Dichlorophenol induces DNA damage through ROS accumulation and GSH depletion in goldfish Carassius auratus.