Peroxidation levels in <i>Eschericia coli</i> as a potential toxicity marker: Effect of nickel and methyl‐parathion

Espigares, M.; Lucadamo, Lucio; Coca, C.; Aloj, E.; Gálvez, Ramón

doi:10.1002/tox.2530090307

Cited by 4 publications

(5 citation statements)

References 30 publications

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“…Studies are implicated in the induction of oxidative stress, depletion of endogenous antioxidants, and inhibition of Ni‐induced mitochondrial function in the triggering of Ni‐induced lung, heart, kidney, liver, and brain toxicity 89–92 . Ni could lead to increased cell peroxidation 93 . Ni nanoparticles mediated HepG2 cell apoptosis via mitochondrial pathway 94 .…”

Section: Discussionmentioning

confidence: 99%

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Decreased thioredoxin reductase 3 expression promotes nickel‐induced damage to cardiac tissue via activating oxidative stress‐induced apoptosis and inflammation

Liu

et al. 2022

Environmental Toxicology

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Thioredoxin reductase 3 (Txnrd3) plays a crucial role in antioxidant and anti-cancer activities, and sperm maturation. The damage of heavy metals, including Nickel (Ni), is the most prominent harm in social development, and hampering Txnrd3 might exacerbate Ni-induced cardiac damage. In this study, a total of 160 8-week-old C57BL/N male mice with 25-30 g weight of Txnrd3+/+ wild-type and Txnrd3À/À homozygote-type were randomly divided into eight groups. The mice in the control and Ni groups were gavaged with distilled water and a freshly prepared 10 mg/kg NiCl 2 solution. Melatonin (Mel) groups were administered at a concentration of 2 mg/kg for 21 days at the mice's 0.1 ml/10 g body weight. Ni exposure up-regulated the messenger RNA (mRNA) levels of mitochondrial apoptosis (caspase-3, caspase-9, cytochrome c, p53, and BAX), autophagy (LC3, ATG 1, ATG 7, and Beclin-1), and inflammation (TNF-α, COX 2, IL-1β, IL-2, IL-6, and IL-7)-related markers, but downregulated the mRNA levels of BCL-2, p62 and mTOR (p < .05). Ni exposure decreased the expression of BCL-2 and p62 protein but increased the expression levels of caspase-3, caspase-9, cytochrome c, p53, BAX, ATG 7, Beclin-1, TNF-α, COX 2, IL-1β and IL-2 protein (p < .05). Ni increased the contents of glutathione disulfide (GSSG) and malondialdehyde (MDA) and decreased the activities of catalase (CAT) and total superoxide dismutase (T-SOD) (p < .05). Decreased Txnrd3 expression significantly exacerbated changes compared to the Ni exposure (p < .05). Mel significantly attenuated these changes, but the effect decreased when Txnrd3 was inhibited (p < .05). In conclusion, decreased Txnrd3 expression promoted Ni-induced mitochondrial apoptosis and inflammation via oxidative stress and aggravated heart damage in mice. Decreased Txnrd3 expression significantly reduced the protective effect of Mel to Ni exposure.

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Section: Discussionmentioning

confidence: 99%

“…85 [89][90][91][92] Ni could lead to increased cell peroxidation. 93 Ni nanoparticles mediated HepG2 cell apoptosis via mitochondrial pathway. 94 However, the specific mechanism of Ni-induced heart damage is not…”

Section: Effects Of Decreased Txnrd3 Expression Onmentioning

confidence: 97%

Decreased thioredoxin reductase 3 expression promotes nickel‐induced damage to cardiac tissue via activating oxidative stress‐induced apoptosis and inflammation

Liu

et al. 2022

Environmental Toxicology

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“…These findings also suggest, in accordance with the conclusions of Ž . Espigares et al 1994 , that the TBA-reactive substances in bacteria may constitute a good toxicity marker. The increased saturatedrunsaturated fatty Ž .…”

Section: Discussionmentioning

confidence: 99%

“…grL peptone Espigares et al, 1994 in a water bath at Ž 37ЊC with agitation. In a dose-response study, 2,4-D 2…”

Section: Culture Conditionsmentioning

confidence: 99%

Effect of 2,4-dichlorophenoxyacetic acid herbicide onEscherichia coli growth, chemical composition, and cellular envelope

et al. 2001

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2,4-Dichlorophenoxyacetic acid (2,4-D) is a herbicide widely used in the world and mainly excreted by the renal route in exposed humans and animals. Herbicides can affect other nontarget organisms, such as Escherichia coli. We observed that a single exposure to 1 mM 2,4-D diminished growth and total protein content in all E. coli strains tested in vitro. In addition, successive exposures to 0.01 mM 2,4-D had a toxic effect decreasing growth up to early stationary phase. Uropathogenic E. coli adhere to epithelial cells mediated by fimbriae, adhesins, and hydrophobic properties. 2,4-D exposure of uropathogenic E. coli demonstrated altered hydrophobicity and fimbriation. Hydrophobicity index values obtained by partition in p-xylene/water were 300-420% higher in exposed cells than in control ones. Furthermore, values of hemagglutination titer, protein contents in fimbrial crude extract, and electron microscopy demonstrated a significant diminution of fimbriation in treated cells. Other envelope alterations could be detected, such as lipoperoxidation, evidenced by decreased polyunsaturated fatty acids and increased lipid degradation products (malonaldehyde), and motility diminution. These alterations decreased cell adherence to erythrocytes, indicating a diminished pathogenic capacity of the 2,4-D-exposed E. coli.

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“…One such bioassay is a biotest based on the Ž . inhibition of growth of Escherichia coli IGEC that is extremely simple and that allows the toxicity of various Ž substances to be evaluated Espigares and Mariscal, 1989;Espigares et al, 1990Espigares et al, , 1994Odberg-Ferragut . et al, 1991 . In our study, the IGEC biotest and the acetylcholinesterase inhibition test were applied to a group of newly synthesized DTCs with possible public health applications in order to assess toxicity and formulate conclusions as to the degree of comparative toxicity of the different substances.…”

mentioning

confidence: 99%

In vitro evaluation of the toxicity of several dithiocarbamates using anEscherichia coli growth inhibition bioassay and the acetylcholinesterase inhibition test

Espigares¹,

Crovetto²,

Gálvez³

1998

Environ. Toxicol. Water Qual.

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The industrial and sanitary use of dithiocarbamates DTCs is on the rise, and the synthesis of new derivatives has increased the field of their application. Both positive and negative pharmacological and toxicological effects have been documented for DTCs. The development and application of new 50 exhibited a minimal inhibitory effect on AChE, the results obtained indicate a generalized absence of AChE inhibition for the DTCs.

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Peroxidation levels in Eschericia coli as a potential toxicity marker: Effect of nickel and methyl‐parathion

Cited by 4 publications

References 30 publications

Decreased thioredoxin reductase 3 expression promotes nickel‐induced damage to cardiac tissue via activating oxidative stress‐induced apoptosis and inflammation

Decreased thioredoxin reductase 3 expression promotes nickel‐induced damage to cardiac tissue via activating oxidative stress‐induced apoptosis and inflammation

Effect of 2,4-dichlorophenoxyacetic acid herbicide onEscherichia coli growth, chemical composition, and cellular envelope

In vitro evaluation of the toxicity of several dithiocarbamates using anEscherichia coli growth inhibition bioassay and the acetylcholinesterase inhibition test

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