Apoptotic and Degenerative Changes in the Enteric Nervous System Following Exposure to Fluoride During Pre- and Post-natal Periods

Sarwar, Saba; Quadri, Javed Ahsan; Kumar, Manoj; Singh, Seema; Das, Prasenjit; Nag, Tapas Chandra; Shariff, A

doi:10.1007/s12011-020-02249-x

Cited by 4 publications

(1 citation statement)

References 44 publications

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“…When ROS is used as a signal of oxidative stress, the increase of intracellular reactive oxygen species (ROS) can activate the signal pathway of apoptosis. Once the apoptosis stimulus signal is present, excessive ROS production contributes to macromolecular oxidation, leading to free radicals attacking membrane phospholipids, leading to membrane damage by inducing lipid peroxidation, mitochondrial membrane depolarization, and apoptosis ( 38 ). Mitochondria is both ROS targets and sources of additional ROS production.…”

Section: Potential Molecular Mechanism Of Mitochondrial Dysfunction I...mentioning

confidence: 99%

Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism

Wei

Ali

et al. 2022

Front. Vet. Sci.

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Fluoride is commonly found in the soil and water environment and may act as chronic poison. A large amount of fluoride deposition causes serious harm to the ecological environment and human health. Mitochondrial dysfunction is a shared feature of fluorosis, and numerous studies reported this phenomenon in different model systems. More and more evidence shows that the functions of mitochondria play an extremely influential role in the organs and tissues after fluorosis. Fluoride invades into cells and mainly damages mitochondria, resulting in decreased activity of mitochondrial related enzymes, weakening of protein expression, damage of respiratory chain, excessive fission, disturbance of fusion, disorder of calcium regulation, resulting in the decrease of intracellular ATP and the accumulation of Reactive oxygen species. At the same time, the decrease of mitochondrial membrane potential leads to the release of Cyt c, causing a series of caspase cascade reactions and resulting in apoptosis. This article mainly reviews the mechanism of cytotoxicity related to mitochondrial dysfunction after fluorosis. A series of mitochondrial dysfunction caused by fluorosis, such as mitochondrial dynamics, mitochondrial Reactive oxygen species, mitochondrial fission, mitochondrial respiratory chain, mitochondrial autophagy apoptosis, mitochondrial fusion disturbance, mitochondrial calcium regulation are emphasized, and the mechanism of the effect of fluoride on cytotoxicity related to mitochondrial dysfunction are further explored.

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Section: Potential Molecular Mechanism Of Mitochondrial Dysfunction I...mentioning

confidence: 99%

Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism

Wei

Ali

et al. 2022

Front. Vet. Sci.

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Impact of heavy metals, oxidative stress, expression of VHL, and antioxidant genes in the pathogenesis of renal cell carcinoma

Arulraj,

Quadri,

Nayak

et al. 2024

Urologic Oncology: Seminars and Original Investigations

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Antagonistic role of barley against bioaccumulation and oxidative stress of aflatoxin B1 in male rats

Elgohary

Abdel-Fattah

Abu-Sree

et al. 2022

JoBAZ

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Background This study aims to evaluate the protective effect of barley against the bioaccumulation and oxidative stress of aflatoxin B1 (AFB1) in male rats. The lethality percentile doses (LDs: LD1 to LD99 at 24, 48, 72, and 96 h) were measured. To achieve these goals during subacute treatments, one hundred rats were divided into five groups, each with twenty rats. The groups I, II, III, IV, and V throughout 21 days were daily given drinking water, DMSO, 2.0 g of barley/kg, and 7.49 mg/kg of AFB1 alone or in combination with 2.0 g of barley/kg, respectively. Results The results revealed that AFB1 was detected only in the liver, kidney, and serum of groups IV, in which the accumulated AFB1 exhibited a significant direct relationship with the experimental periods with a marked positive correlation coefficient. Additionally, the concentrations of AFB1 residue in the serum of rats given AFB1 alone exhibited a significant inverse relationship with the levels of GSH, activity of CAT, SOD, and GR, whereas the levels of MDA showed a significant positive relationship. In the serum of rats given AFB1 plus barley, all parameters were mostly recovered and didn’t correlate with either the experimental periods or AFB1 in the serum. Conclusions The present data concluded that barley accelerated the biotransformation of AFB1 to a hydrophilic metabolite that is easily eliminated outside the body, leading to the recovery of all studied parameters to normal levels.

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Apoptotic and Degenerative Changes in the Enteric Nervous System Following Exposure to Fluoride During Pre- and Post-natal Periods

Cited by 4 publications

References 44 publications

Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism

Effect of Fluoride on Cytotoxicity Involved in Mitochondrial Dysfunction: A Review of Mechanism

Impact of heavy metals, oxidative stress, expression of VHL, and antioxidant genes in the pathogenesis of renal cell carcinoma

Antagonistic role of barley against bioaccumulation and oxidative stress of aflatoxin B1 in male rats

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