Reactive oxygen species in developmental toxicity: Review and hypothesis

Fantel, Alan G.

doi:10.1002/(sici)1096-9926(199603)53:3<196::aid-tera7>3.0.co;2-2

Cited by 152 publications

(88 citation statements)

References 172 publications

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“…At present, there are no data relating teratogen-induced cell death in embryos and the mitochondrial events just described. Nonetheless, this mitochondrial signaling pathway may play an important role in teratogen-induced cell death because (1) a variety of teratogens are known to induce ROS levels in exposed embryos (Fantel, 1996), (2) mitochondria are the primary site for the generation of reactive oxygen species (ROS) (Halliwell and Gutteridge, 1989), and (3) ROS have been implicated in the induction of apoptosis (Buttke and Sandstrom, 1994).…”

Section: Discussionmentioning

confidence: 99%

Teratogen-induced cell death in postimplantation mouse embryos: differential tissue sensitivity and hallmarks of apoptosis

Mirkes

Little

1998

Cell Death Differ

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Teratogen-induced cell death is a common event in the pathogenesis associated with tissues destined to be malformed. Although the importance of this cell death is recognized, little information is available concerning the biochemistry of teratogen-induced cell death. We show that three teratogens, hyperthermia, cyclophosphamide and sodium arsenite induce an increase in cell death in day 9.0 mouse embryos with concurrent induction of DNA fragmentation, activation of caspase-3 and the cleavage of poly (ADPribose) polymerase (PARP). Teratogen-induced cell death is also selective, i.e., some cells within a tissue die while others survive. In addition, cells within some tissues die when exposed to teratogens while cells in other tissues are relatively resistant to teratogen-induced cell death. An example of the latter selectivity is seen in the cells of the developing heart, which are resistant to the cytotoxic potential of many teratogens. We show that the absence of cell death in the heart is accompanied by the complete lack of DNA fragmentation, activtion of caspase-3 and the cleavage of PARP.

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Section: Discussionmentioning

confidence: 99%

Teratogen-induced cell death in postimplantation mouse embryos: differential tissue sensitivity and hallmarks of apoptosis

Mirkes

Little

1998

Cell Death Differ

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“…DCFDA is reactive to HO·, RO·, ROO· and H 2 O 2 in the presence of cellular peroxidases [88]. Oxidative stress can also be assessed by measuring lipid peroxidation C11-BIODIPY assay and TBA assay for malondialdehyde [89]. Availability of numerous other assays makes the assessment much convenient.…”

Section: Oxidative Stress Assaymentioning

confidence: 99%

In vitro and in vivo toxicity assessment of nanoparticles

2017

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Nanotechnology has revolutionized gene therapy, diagnostics and environmental remediation. Their bulk production, uses and disposal have posed threat to the environment. With the appearance of these nanoparticles in the environment, their toxicity assessment is an immediate concern. This review is an attempt to summarize the major techniques used in cytotoxity determination. The review also presents a detailed and elaborative discussion on the toxicity imposed by different types of nanoparticles including carbon nanotubes, gold nanoparticles, silver nanoparticles, quantum dots, fullerenes, aluminium nanoparticles, zinc nanoparticles, iron nanoparticles, titanium nanoparticles and silica nanoparticles. It discusses the in vitro and in vivo toxological effects of nanoparticles on bacteria, microalgae, zebrafish, crustacean, fish, rat, mouse, pig, guinea pig, human cell lines and human. It also discusses toxological effects on organs such as liver, kidney, spleen, sperm, neural tissues, liver lysosomes, spleen macrophages, glioblastoma cells, hematoma cells and various mammalian cell lines. It provides information about the effects of nanoparticles on the gene-expression, growth and reproduction of the organisms.

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“…Every year number of new studies are reported explaining different mechanisms related to toxic actions of 2,4-D, a common herbicide on plants, animals and human cells (Fantel 1996;Don-Pedro 1996;Coppen and Jepsons 1996;Schrader et al 1999;Heiden et al 2006;Hardell 2008;Cogliano et al 2011;Mortensen et al 2012;Von Stackelberg 2013;Song 2014). Degradation by soil micro organisms is assumed as main cause of 2,4-D decomposition in soil.…”

mentioning

confidence: 99%

“…At present it is well known that 2,4-D can disturb some chemical reactions by interacting with phospholipids generating free radicals causing lipid peroxidation. It also binds to enzymes resulting in change of their activity (Fantel 1996;Don-Pedro 1996). Increased lipid peroxidation and oxidative stress can affect the activities of protective enzymatic antioxidants that have been shown to be sensitive indicators of increased oxidation reactions (Fantel 1996;Schrader et al 1999).…”

mentioning

confidence: 99%

Does 2,4-dichlorophenoxyacetic acid (2,4-D) induce genotoxic effects in tissue cultured Allium roots?

et al. 2016

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2,4-Dichlorophenoxyacetic acid (2,4-D) is a synthetic plant growth regulator that is highly toxic to most broad leaved plants and relatively nontoxic to monocotyledonous plants; is frequently used as weed killer. The study aimed to investigate cytogenetic effects of different concentrations of 2,4-D (0.67, 1.34, 2.01, 2.68, 3.35 and 4.02 mg/L) on Allium cepa bulblets' root tips treated for 24 and 48 h. The results showed six types of structural aberrations: C-mitosis, stickiness, laggards, bridges, fragments and multipolarity that varied numerically compared to control. It significantly affected mitotic index (MI) at 24 and 48 h treatment. In the Allium test, MI increased significantly at three lower concentrations (0.67, 1.34, 2.01 mg/L) after treatment with 2,4-D for 24 h and decreased significantly at higher concentration. Whereas, 2,4-D treatment for 48 h increased MI at all concentrations with significantly decreased MI at the highest concentration. The experiment was extended using comet test that did not reveal significant difference among treatments except for application of 4.02 mg/L 2,4-D for 48 h; where cell damages were verified by comet test. Rest of the concentrations for any duration of time were not damaging and toxic to cells. The results showed, visible mitodepressive action of 4.02 mg/L 2,4-D when treated for 48 h that had tendency to become toxic if the roots had been in touch with 2,4-D for a longer time.

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Reactive oxygen species in developmental toxicity: Review and hypothesis

Cited by 152 publications

References 172 publications

Teratogen-induced cell death in postimplantation mouse embryos: differential tissue sensitivity and hallmarks of apoptosis

Teratogen-induced cell death in postimplantation mouse embryos: differential tissue sensitivity and hallmarks of apoptosis

In vitro and in vivo toxicity assessment of nanoparticles

Does 2,4-dichlorophenoxyacetic acid (2,4-D) induce genotoxic effects in tissue cultured Allium roots?

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