The protective effect of melatonin on benzo(a)pyrene-induced brain injury: role of apoptosis and autophagy pathways

Mehri, Soghra; Barangi, Samira; Zamiri, Ehsan; Karimi, Gholamreza

doi:10.1007/s00210-020-01936-9

Cited by 19 publications

(17 citation statements)

References 67 publications

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“…Furthermore, studies on the therapeutic approach to mitigate PAH-induced neurotoxicity were also considered in the last decade. A study showed that melatonin exhibited neuroprotection against benzo[a]pyrene induced neuronal oxidative stress, neuronal death and autophagy [ 46 ]. The study of Mohanty et al [ 47 ] also revealed the role of retinoic acid as a possible therapeutic intervention against benzo[a]pyrene induced neurotoxicity via attenuation of oxidative damage to the brain and mitigation of neurobehavioral and neuromorphological deficits in a zebrafish model.…”

Section: Discussionmentioning

confidence: 99%

“…Lin et al [ 48 ] reported the molecular basis of benzo[a]pyrene-induced neurotoxicity during embryogenesis in zebrafish via upregulation of oxidative stress related genes ( sod1 , sod2 and cyp1a1 ) and increase in malondialdehyde production. Other studies also established that benzo[a]pyrene disrupted brain antioxidant defence systems in vitro and in vivo by triggering lipid peroxidation and inhibiting antioxidant enzymes [ 46 , 49 , 50 ]. High levels of malondialdehyde and a weak antioxidant defence system have been linked to radical-induced neuronal damage and neurodegeneration [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

“…Some of the articles retrieved from the databases showed a link between neuronal apoptosis and autophagy and benzo[a]pyrene-induced neurotoxicity. One of the authors established that benzo[a]pyrene induced neuronal death via disruption of apoptotic markers and autophagy proteins [ 46 ]. The study showed that exposure to 75 mg/kg of benzo[a]pyrene upregulated cleaved caspase-3 activity but did not alter the level of pro-caspase 3 and Bcl-2 in the mouse brain.…”

Section: Discussionmentioning

confidence: 99%

“…Neuroprotective potentials of retinoic acid against benzo[a]pyrene-induced neurotoxicity were associated with different biochemical mechanisms, including reduction of malondialdehyde and protein carbonyl production, activation of antioxidant enzymes, inhibition of neuronal pyknosis and prevention of behavioural alteration. A recent study revealed that melatonin also exhibited neuroprotection against benzo[a]pyrene-induced neurotoxicity via reduction of apoptotic markers and inhibition of neuronal apoptosis and autophagy [ 46 ]. The report of Saha et al [ 95 ] also showed that a medicinal plant, Bacopa monnieri , may provide beneficial effects against PAH-induced neurological deficit.…”

Section: Discussionmentioning

confidence: 99%

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Neurotoxicity of Polycyclic Aromatic Hydrocarbons: A Systematic Mapping and Review of Neuropathological Mechanisms

Olasehinde

Olaniran

2022

Toxics

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Several studies present the neurotoxic effects of polycyclic aromatic hydrocarbons (PAHs), a class of environmental pollutants capable of causing neurological deficits. However, a collective review approach to this research topic is scarce. This study presents the effect of PAHs on the central nervous system using a bibliometric approach. The neuropathological mechanisms of PAHs are also highlighted. Published articles were searched for in the Scopus and Web of Science databases from January 1979 to December 2020 using the keywords ‘polycyclic aromatic hydrocarbons’ and ‘neurotoxicity’. The total number of documents retrieved from both databases was 338. Duplicated documents (80) were excluded and 258 articles were used for the final analysis. Our findings revealed that there has been a significant increase in research outputs on this topic in the last ten years. The countries with the highest scientific productivity in this area are USA, China, France and Italy. The result also showed that, in the past few years, global scientific output in research relating to PAH neurotoxicity focused on neurodegeneration, cholinergic function, neurodevelopmental toxicity, behavioural studies, oxidative stress, neuroprotection and therapeutic intervention using different experimental models, including zebrafish, neuronal cell lines, Caenorhabditis elegans and rats. Recent studies also revealed the neuroprotective roles of some natural products against PAH-induced neurotoxicity. However, more investigation involving clinical trials is required to emphasize the observed neurotoxic effects.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Neurotoxicity of Polycyclic Aromatic Hydrocarbons: A Systematic Mapping and Review of Neuropathological Mechanisms

Olasehinde

Olaniran

2022

Toxics

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“…Steatosis is a common liver disease with a significant accumulation of fats or carbohydrates in countries with Western diets (Uno et al, 2018). Compounds that have antioxidant and anti‐inflammatory properties are able to protect the liver from damage caused by reactive metabolites (Deng et al, 2020; Mehri, Barangi, Zamiri, & Karimi, 2020; Rangi et al, 2018). We reported in the recent study that ATV can reduce BaP‐induced ovarian toxicity by reducing oxidative stress (Rahmani, Karimpour Malekshah, Zargari, & Talebpour, 2021).…”

Section: Introductionmentioning

confidence: 99%

Hepatotoxicity in young adult rat offspring after prenatal exposure to benzo(a)pyrene, and protective effect of atorvastatin

Malekshah

Rahmani

Zargari

et al. 2022

Birth Defects Research

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Objectives: Benzo[a]pyrene (BaP) is an environmental contaminant that interrupts the antioxidant defense and thus leads to oxidative stress and DNA damage in the liver. Atorvastatin (ATV) for reducing cholesterol has antioxidant and anti-apoptotic activities. This study investigated the effects of prenatal exposure of BaP on liver toxicity and the protective role of ATV in reducing liver toxicity. Materials and Methods:In this study, rats were distributed randomly to seven groups: I. Saline control; II. ATV (10 mg/kg); III. Corn oil; IV and V. BaP (10 and 20 mg/kg); VI and VII. ATV + BaP (10 and 20 mg/kg). BaP and ATV were administrated from gestation day 7-16 (GD7-GD16), orally. Ten weeks after the birth, female offspring were examined for oxidative stress markers, liver enzymes, and histology. Results: Data revealed that BaP significantly induced oxidative stress (decreased glutathione and increased malondialdehyde level), and disrupted the tissue structure of the liver. Moreover, alanine aminotransferase, aspartate aminotransferase, and alkaline phosphatase increased in the offspring. ATV treatment along with BaP during gestation was able to bring the antioxidant status and serum liver enzymes levels relatively close to normal. As well as, histological findings showed that ATV was able to improve liver tissue structure caused by BaP. Conclusion:Based on the above studies we concluded that ATV at a low dose during gestation was able to reduce liver damage caused by BaP with antioxidant properties.

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The modulation of SIRT1 and SIRT3 by natural compounds as a therapeutic target in doxorubicin‐induced cardiotoxicity: A review

Tabrizi

Yarmohammadi

Hayes

et al. 2021

J Biochem & Molecular Tox

Self Cite

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Doxorubicin (DOX) is a potent antitumor agent with a broad spectrum of activity; however, irreversible cardiotoxicity resulting from DOX treatment is a major issue that limits its therapeutic use. Sirtuins (SIRTs) play an essential role in several physiological and pathological processes including oxidative stress, apoptosis, and inflammation. It has been reported that SIRT1 and SIRT3 can act as a protective molecular against DOX-induced myocardial injury through targeting numerous signaling pathways. Several natural compounds (NCs), such as resveratrol, sesamin, and berberine, with antioxidative, anti-inflammation, and antiapoptotic effects were evaluated for their potential to suppress the cardiotoxicity induced by DOX via targeting SIRT1 and SIRT3. Numerous NCs exerted their therapeutic effects on DOX-mediated cardiac damage via targeting different signaling pathways, including SIRT1/LKB1/AMPK, SIRT1/PGC-1α, SIRT1/NLRP3, and SIRT3/FoxO. SIRT3 also ameliorates cardiotoxicity by enhancing mitochondrial fusion.

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The protective effect of melatonin on benzo(a)pyrene-induced brain injury: role of apoptosis and autophagy pathways

Cited by 19 publications

References 67 publications

Neurotoxicity of Polycyclic Aromatic Hydrocarbons: A Systematic Mapping and Review of Neuropathological Mechanisms

Neurotoxicity of Polycyclic Aromatic Hydrocarbons: A Systematic Mapping and Review of Neuropathological Mechanisms

Hepatotoxicity in young adult rat offspring after prenatal exposure to benzo(a)pyrene, and protective effect of atorvastatin

The modulation of SIRT1 and SIRT3 by natural compounds as a therapeutic target in doxorubicin‐induced cardiotoxicity: A review

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