Oxidative stress, cholinesterase activity, and DNA damage in the liver, whole blood, and plasma of Wistar rats following a 28-day exposure to glyphosate

Milić, Mirta; Žunec, Suzana; Micek, Vedran; Kašuba, Vilena; Mikolić, Anja; Lovaković, Blanka Tariba; Semren, Tanja Živković; Pavičić, Ivan; Čermak, Ana Marija Marjanović; Pizent, Alica; Vrdoljak, Ana Lucić; Valencia-Quintana, Rafael; Sánchez-Alarcón, Juana; Želježić, Davor

doi:10.2478/aiht-2018-69-3114

Cited by 57 publications

(29 citation statements)

References 73 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The decreased activities of CAT and SOD can be used to indicate the accumulation of superoxide radicals and/or hydroxyl radicals in the liver. GSH, as a nonenzymatic scavenger, can scavenge a wide variety of reactive species [38]. GSH-Px works together with CAT to scavenge excess lipid peroxide and hydrogen, which is helpful for eliminating peroxide during the reaction between GSH and H 2 O 2 [27].…”

Section: Discussionmentioning

confidence: 99%

Copper Induces Oxidative Stress and Apoptosis in the Mouse Liver

Liu

Guo

Jian

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Copper (Cu) is an essential trace element involved in the normal physiological processes of animals. However, excessive exposure to Cu can produce numerous detrimental impacts. The aim of this study was to investigate the effects of Cu on oxidative stress and apoptosis as well as their relationship in the mouse liver. Four-week-old ICR mice (n=240) were randomly assigned to different Cu (Cu2+-CuSO4) treatment groups (0, 4, 8, and 16 mg/kg) for periods of 21 and 42 days. The high doses of Cu exposure could induce oxidative stress, by increasing the levels of reactive oxygen species (ROS) and protein carbonyls (PC) and decreasing the activities of antisuperoxide anion (ASA) and antihydroxyl radical (AHR) and content of glutathione (GSH), as well as activities and mRNA expression levels of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Moreover, high doses of Cu exposure induced hepatic apoptosis via the mitochondrial apoptotic pathway, as characterized by the depolarization of mitochondrial membrane potential (MMP); significantly increased mRNA and protein expression levels of cytosolic cytochrome (Cyt c), apoptosis-inducing factor (AIF), endonuclease G (Endo G), apoptosis protease-activating factor-1 (Apaf-1), cleaved caspase-9, cleaved caspase-3, cleaved PARP, Bcl-2 antagonist killer (Bak), Bcl-2-associated X protein (Bax), and Bcl-2-interacting mediator of cell death (Bim); and decreased mRNA and protein expression levels of B-cell lymphoma-2 (Bcl-2) and Bcl-extra-large (Bcl-xL). Furthermore, the activation of the tumor necrosis factor receptor-1 (TNF-R1) signaling pathway was involved in Cu-induced apoptosis, as characterized by the significantly increased mRNA and protein expression levels of TNF-R1, Fas-associated death domain (FADD), TNFR-associated death domain (TRADD), and cleaved caspase-8. These results indicated that exposure to excess Cu could cause oxidative stress triggered by ROS overproduction and diminished antioxidant function, which in turn promoted hepatic apoptosis via mitochondrial apoptosis and that the TNF-R1 signaling pathway was also involved in the Cu-induced apoptosis.

show abstract

Section: Discussionmentioning

confidence: 99%

Copper Induces Oxidative Stress and Apoptosis in the Mouse Liver

Liu

Guo

Jian

et al. 2020

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…Oxidant-mediated responses, such as apoptotic or necrotic cell death, membrane lipid peroxidation, metabolic perturbation, and deregulation of several signaling pathways) are several well-known toxicological effects of insecticides 93,94 . Hence, the study of antioxidant enzymes has been used as a popular method to evaluate the response of multiple animal models, including rats, mice, fish, and green snake head, under pesticide-induced stress conditions 78,[95][96][97][98][99][100] . In the present study, lufenuron was found to increase the level of MDA and decrease the level of GPx and SOD enzymes in liver cells in mothers and their fetuses in a dose-dependent manner, which refers to the oxidative stress posed by the insecticide on the liver cells of the treated animals.…”

Section: Discussionmentioning

confidence: 99%

Lufenuron induces reproductive toxicity and genotoxic effects in pregnant albino rats and their fetuses

Basal

Ahmed

Mahmoud

et al. 2020

Sci Rep

View full text Add to dashboard Cite

Insecticides and other agrochemicals have become indispensable components of the agricultural system to ensure a notable increase in crop yield and food production. As a natural consequence, chemical residues result in significantly increased contamination of both terrestrial and aquatic ecosystems. The present study evaluated the teratogenic, genotoxic, and oxidative stress effects of residual-level lufenuron exposure on pregnant rats during the organogenesis gestational period of both mother and fetus. The tested dams were divided into three groups; control (untreated), low-dose group (orally administered with 0.4 mg/kg lufenuron) and high-dose group (orally administered with 0.8 mg/kg lufenuron). The dams of the two treatment groups showed teratogenic abnormalities represented by the asymmetrical distribution of fetuses in both uterine horns, accompanied by observed resorption sites and intensive bleeding in the uterine horns, whereas their fetuses suffered from growth retardation, morphologic malformations, and skeletal deformations. Histologic examination of the liver and kidney tissues obtained from mothers and fetuses after lufenuron exposure revealed multiple histopathologic changes. DNA fragmentation and cell cycle perturbation were also detected in the liver cells of lufenuron-treated pregnant dams and their fetuses through comet assay and flow cytometry, respectively. Moreover, lufenuron-induced oxidative stress in the liver of mothers and fetuses was confirmed by the increased malondialdehyde levels and decreased levels of enzymatic antioxidants (glutathione peroxidase and superoxide dismutase). Taken together, it can be concluded that lufenuron has a great potential in exerting teratogenic, genotoxic, and oxidative stresses on pregnant rats and their fetuses upon chronic exposure to residual levels during the organogenesis gestational period. The obtained results in the present study imply that women and their fetuses may have the same risk.

show abstract

“…Data for liver and kidney weights have been more variable. For example, one report indicated decreases in liver weight (Ren et al, ), another increase in organ weights of liver, brain, kidney and heart (Cox, ; El‐Shenawy, ; Milić et al, ), and another study reported no changes in liver weight (Çağlar & Kolankaya, ). The U.S. Environmental Protection Agency (EPA) suggested that they depended on glyphosate concentration and animal species (EPA, ).…”

Section: Discussionmentioning

confidence: 99%

Effect of in ovo glyphosate injection on embryonic development, serum biochemistry, antioxidant status and histopathological changes in newly hatched chicks

Fathi

Abdelghani

Shen

et al. 2019

Animal Physiology Nutrition

View full text Add to dashboard Cite

This study aimed to investigate the potential toxic effects of pure glyphosate or Roundup® on hatchability, serum biochemistry and histopathological observation of the liver and kidney of newly hatched chicks. On day six, a total of 225 fertile eggs were obtained from Huafeng breeder hens. The eggs were randomly divided into three treatments: (a) the control group injected with deionized water, (b) the glyphosate group injected 10 mg pure glyphosate/Kg egg mass and (c) the Roundup group injected 10 mg the active ingredient glyphosate in Roundup®/Kg egg. The results showed a decrease of hatchability rate in chicks treated with Roundup® (66%). In addition, no significant change was observed in body weights, yolk sac weight and relative weight organs except the liver and kidney were significantly increased with groups treated with glyphosate and Roundup® compared to the control group. The results showed that serum protein profiles were linearly significantly increased of serum phosphor, uric acid, aspirate aminotransferase, alanine transaminase and alkaline phosphatase in groups treated with Roundup®, as well as the serum concentrations of triglyceride altered after treatment with glyphosate. Furthermore, oxidative stress was observed in the treated chicks, the glyphosate and Roundup® induced changes of the content of malondialdehyde in both the liver and kidney, moreover decrease of glutathione peroxidase, total superoxide dismutase and catalase activity in the kidney tissue and serum. Additionally, changes also happened in the histomorphology of the liver and kidney tissue of the treated chicks. It can be concluded that Roundup® as a probable decrease of hatchability. Exposure to glyphosate alone or Roundup® caused liver and kidney histopathological alterations, serum parameters imbalances and oxidative stress, also induced a variety of liver and kidney biochemical alterations that might impair normal organ functioning in newly hatched chicks.

show abstract

Oxidative stress, cholinesterase activity, and DNA damage in the liver, whole blood, and plasma of Wistar rats following a 28-day exposure to glyphosate

Cited by 57 publications

References 73 publications

Copper Induces Oxidative Stress and Apoptosis in the Mouse Liver

Copper Induces Oxidative Stress and Apoptosis in the Mouse Liver

Lufenuron induces reproductive toxicity and genotoxic effects in pregnant albino rats and their fetuses

Effect of in ovo glyphosate injection on embryonic development, serum biochemistry, antioxidant status and histopathological changes in newly hatched chicks

Contact Info

Product

Resources

About