Oxidative damage in the liver and brain of the rats exposed to frequency-dependent radiofrequency electromagnetic exposure: biochemical and histopathological evidence

Sharma, Anjali; Shrivastava, Sadhana; Shukla, Sangeeta

doi:10.1080/10715762.2021.1966001

Cited by 8 publications

(5 citation statements)

References 51 publications

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“…LPO generated after exposure to D-GalN and LPS depleted various antioxidant enzymes, which gradually damaged hepatorenal tissues. [57] The enzymes responsible for balancing the GSH cycle during increased oxidative stress are GPx, GR, G6PDH, and G-S-T. Oxidation of GSH into GSSG by GPx releases protons to neutralize various ROS produced after exposure to D-GalN and LPS. [57] Enzyme GR converted GSSG into GSH using NADPH as a source of the electron, and G6PDH reduced NADP + into NADPH to make it available again for GR.…”

Section: Discussionmentioning

confidence: 99%

“…[57] The enzymes responsible for balancing the GSH cycle during increased oxidative stress are GPx, GR, G6PDH, and G-S-T. Oxidation of GSH into GSSG by GPx releases protons to neutralize various ROS produced after exposure to D-GalN and LPS. [57] Enzyme GR converted GSSG into GSH using NADPH as a source of the electron, and G6PDH reduced NADP + into NADPH to make it available again for GR. [57] The enzyme G-S-T actively scavenged cytotoxic and genotoxic metabolites of D-GalN and LPS with the help of GSH and reduced peroxides burden in tissues.…”

Section: Discussionmentioning

confidence: 99%

“…[ 57 ] Enzyme GR converted GSSG into GSH using NADPH as a source of the electron, and G6PDH reduced NADP + into NADPH to make it available again for GR. [ 57 ] The enzyme G‐S‐T actively scavenged cytotoxic and genotoxic metabolites of d ‐GalN and LPS with the help of GSH and reduced peroxides burden in tissues. [ 58 ] Increased production of ROS due to the exposure to d ‐GalN and LPS decreased the level of SOD and catalase.…”

Section: Discussionmentioning

confidence: 99%

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Protective activity of purpurin against d‐galactosamine and lipopolysaccharide‐induced hepatorenal injury by upregulation of heme oxygenase‐1 in the RBC degradation cycle

Rakshit

Sahu

Nirala

et al. 2022

J Biochem & Molecular Tox

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Acute liver failure, associated with oxidative stress and sustained inflammation is the major clinical manifestation of liver diseases with a high mortality rate due to limited therapeutic options. Purpurin is a bioactive compound of Rubia cordifolia that has been used in textile staining, as a food additive, and as a treatment of multiple chronic and metabolic diseases associated with inflammation and oxidative stress. The present work aimed to investigate the protective efficacy of purpurin against hepatorenal damage. Thirty‐six female albino rats were equally assigned into six groups. Purpurin was administered orally once a day for 6 days at doses of 05, 10, and 20 mg/kg, respectively. Intraperitoneal injection of lipopolysaccharide (50 μg/kg) was administered to the animals on 6th day evening, 1 h after d‐galactosamine (300 mg/kg) administration to induce hepatorenal injury. The results revealed that purpurin alleviated alterations in serological and hematological parameters as well as restored histoarchitectural and cellular integrity of the liver and kidney. Purpurin restored superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase, and glutathione content in hepatorenal tissues. Accompanied by the diminution of increased bilirubin and biliverdin, purpurin also diminished total cholesterol, triglyceride, and lipid peroxidation in hepatorenal tissues. Purpurin markedly attenuated the elevation of CYP2E1, restored glutathione‐S‐transferase, and prevented DNA damage in hepatorenal tissues. Purpurin reduced iron overload by reducing heme depletion and recycling of ferritin and hemosiderin. It also reinforced biliverdin reductase, heme oxygenase‐1 to employ hepatorenal protection by regulating antioxidant enzymes and other pathways that produced NADPH. Thus, it may be concluded that purpurin has protective potential against acute hepatorenal injury.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Protective activity of purpurin against d‐galactosamine and lipopolysaccharide‐induced hepatorenal injury by upregulation of heme oxygenase‐1 in the RBC degradation cycle

Rakshit

Sahu

Nirala

et al. 2022

J Biochem & Molecular Tox

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“…Radiation exposure, a common environmental physical factor known for its double-edged ability to provide beneficial or non-beneficial outcomes, is used in medical diagnosis or therapy and can improve the liver immune function at low radiation doses ( Zhang et al, 2021a ). However, there is also a risk of oxidative liver damage after frequent high doses of radiotherapy ( Sharma et al, 2021 ). The molecular pathogenic mechanisms of radiation-induced liver injury remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Potential role of gut microbiota-LCA-INSR axis in high fat-diet-induced non-alcoholic fatty liver dysfunction: From perspective of radiation variation

Pan

Zhou

Zhao

et al. 2022

Current Research in Food Science

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“…экспериментальные животные (крысы) подвергались воздействию частот 900, 1800 и 2100 МГц по часу в день в течении месяца. Гистопатологические исследования показали тяжелые дегенеративные изменения в ткани печени -инфильтрацию центри лобулярных мононуклеарных клеток, окислительное повреждение печени [16].…”

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Influence of Radiofrequency Electromagnetic Field Radiation on the Liver of Rats

SIKHARULIDZE¹,

SUMBADZE²,

KORDZAIA³

2022

jecm

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The modern development of civilization cannot be imagined without the constantly growing number of many devices that emit electromagnetic waves. Mobile phones as sources of electromagnetic field (EMF) belong to the low radio frequency range. All this is of great interest for studying the influence of radio frequencies as an artificially created environmental factor on the health of humans and other living organisms. According to an experimental study, the impact of this radio frequency range on the liver causes damage to this organ. In particular, histo-pathological, degenerative changes in the liver parenchyma, significant biochemical functional changes, oxidative stress, and genetic damage to hepatocytes were revealed. All this suggests that similar changes can occur in the human body, which is the subject of further research

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Oxidative damage in the liver and brain of the rats exposed to frequency-dependent radiofrequency electromagnetic exposure: biochemical and histopathological evidence

Cited by 8 publications

References 51 publications

Protective activity of purpurin against d‐galactosamine and lipopolysaccharide‐induced hepatorenal injury by upregulation of heme oxygenase‐1 in the RBC degradation cycle

Protective activity of purpurin against d‐galactosamine and lipopolysaccharide‐induced hepatorenal injury by upregulation of heme oxygenase‐1 in the RBC degradation cycle

Potential role of gut microbiota-LCA-INSR axis in high fat-diet-induced non-alcoholic fatty liver dysfunction: From perspective of radiation variation

Influence of Radiofrequency Electromagnetic Field Radiation on the Liver of Rats

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