Hesperidin and hesperetin against heavy metal toxicity: Insight on the molecular mechanism of mitigation

Famurewa, Ademola C.; Renu, Kaviyarasi; Eladl, Mohamed Ahmed; Chakraborty, Rituraj; Myakala, Haritha; El‐Sherbiny, Mohamed; Elsherbini, Dalia Mahmoud Abdelmonem; Vellingiri, Balachandar; Madhyastha, Harishkumar; Wanjari, Uddesh Ramesh; Mukherjee, Anirban Goutam; Gopalakrishnan, Abilash Valsala

doi:10.1016/j.biopha.2022.112914

Cited by 49 publications

(19 citation statements)

References 187 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Environmental toxicants are ubiquitous and have been implicated in the pathophysiology of chronic diseases and organ damage (Famurewa et al, 2022). Carbon tetrachloride is among these environmental pollutants that inadvertently enter the human body and trigger pathologies.…”

Section: Introductionmentioning

confidence: 99%

Hepatoprotective Mechanism of Apigenin via Suppression of Oxidative Inflammatory Signaling and Apoptosis against Hepatotoxicity Induced by CCl4 in Rats

Alabbad¹,

Alfwuaires²,

Abdel‐Moneim³

et al. 2023

IJAR

View full text Add to dashboard Cite

Background: Carbon tetrachloride (CCl4) is a critical hepatotoxicant causing liver injury and fibrosis via hepatic production of reactive oxygen species (ROS). Apigenin (APG) is a natural bioactive compound and flavonoid antioxidant. We, therefore, evaluated whether APG could mitigate CCl4-mediated hepatotoxicity. Methods: Rats were randomly divided and administered APG and/or CCl4 in Control group, CCl4 group, APG + CCl4 groups (APG: 10 and 20 mg/kg bw) and APG groups (APG: 10 and 20 mg/kg bw) 2 times per week for 7 consecutive weeks. Result: Rats exposed to CCl4 demonstrated marked increases in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and monoamine oxidase (MAO) activities and decreased hepatic malondialdehyde (MDA) level compared to control. The hepatic activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) decreased appreciably. The CCl4 intoxication caused significant increases in inflammatory cytokines (IL-6 and TNF-α) and apoptosis markers, while the anti-inflammatory cytokines (IL-4 and IL-10) decreased with evident histopathological lesions compared to control. APG-dose-dependently-prevented these hepatic alterations.

show abstract

Section: Introductionmentioning

confidence: 99%

Hepatoprotective Mechanism of Apigenin via Suppression of Oxidative Inflammatory Signaling and Apoptosis against Hepatotoxicity Induced by CCl4 in Rats

Alabbad¹,

Alfwuaires²,

Abdel‐Moneim³

et al. 2023

IJAR

View full text Add to dashboard Cite

show abstract

“…Physiologically, SOD detoxifies superoxide radicals; CAT catalyzes the reaction that drives the lysis of H 2 O 2 to H 2 O and molecular O 2 . Whereas, GPx, a tripeptide peroxidase mediates the neutralization of peroxyl radicals through the reducing action of its glutathione (GSH) moiety [49]. Therefore, DM-induced depression in the testicular activities of SOD, CAT, and GPx would consequently result into testicular oxidative stress [24,47] and degeneration of testicular ultrastructure which might have contributed to decreased testis weight herein (Table 1).…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Mitigates Diabetic Testicular Dysfunction, Endocrine Deficits, and Insulin Resistance via Suppression of Sperm-Endocrine Aberrations and Oxidative Inflammation in Rats

Famurewa

Sedky

2023

Andrologia

Self Cite

View full text Add to dashboard Cite

Diabetes mellitus (DM) provokes reproductive impairments through endocrine disturbance, sperm deficits, and testicular oxidative inflammation. The study investigated the reproductive protective effects of resveratrol (RSV) against testicular oxidative inflammation, sperm/endocrine deficits, and insulin resistance in streptozotocin- (STZ-, 65 mg/kg) induced DM rat model. Male rats were randomly divided into 4 groups ( n = 6 ): control, DM, RSV (150 mg/kg bw, orally), and RSV+DM group (21 days). The nontreated DM rats showed marked decreases in serum insulin, reproductive hormones (T, LH, and FSH), and lipid profile levels compared to control. The homeostatic index of insulin resistance (HOMA-IR) and the quantitative insulin sensitivity check index (QUICKI) were adversely modulated. Sperm count and motility were profoundly decreased, whereas sperm abnormality was significantly increased. The testicular activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and malondialdehyde (MDA) level, along with inflammatory cytokines (TNF-α, IL-6, IL-4, and IL-10) were significantly dysregulated. The DM induced histopathological lesions compared to control rats. Interestingly, the RSV administration to DM rats attenuated the altered reproductive parameters, restored antioxidant mechanism, and anti-inflammatory responses with improved insulin resistance. RSV could prevent DM-induced reproductive deficits and insulin resistance via modulating oxidative stress-mediated testicular inflammation in rats.

show abstract

“…As one of the most dangerous and ubiquitous environmental contaminants, Pb affects all biological systems when it comes into contact with food, drink, and air ( 76 ). Exposure to Pb causes clinical pathological changes by raising toxicity in the endocrine system and the kidney ( 77 ).…”

Section: Heavy Metals: Their Toxicity Mechanism and Effectsmentioning

confidence: 99%

A review of important heavy metals toxicity with special emphasis on nephrotoxicity and its management in cattle

Tahir

Alkheraije

2023

Front. Vet. Sci.

View full text Add to dashboard Cite

Toxicity with heavy metals has proven to be a significant hazard with several health problems linked to it. Heavy metals bioaccumulate in living organisms, pollute the food chain, and possibly threaten the health of animals. Many industries, fertilizers, traffic, automobile, paint, groundwater, and animal feed are sources of contamination of heavy metals. Few metals, such as aluminum (Al), may be eliminated by the elimination processes, but other metals like lead (Pb), arsenic (As), and cadmium (Ca) accumulate in the body and food chain, leading to chronic toxicity in animals. Even if these metals have no biological purpose, their toxic effects are still present in some form that is damaging to the animal body and its appropriate functioning. Cadmium (Cd) and Pb have negative impacts on a number of physiological and biochemical processes when exposed to sub-lethal doses. The nephrotoxic effects of Pb, As, and Cd are well known, and high amounts of naturally occurring environmental metals as well as occupational populations with high exposures have an adverse relationship between kidney damage and toxic metal exposure. Metal toxicity is determined by the absorbed dosage, the route of exposure, and the duration of exposure, whether acute or chronic. This can lead to numerous disorders and can also result in excessive damage due to oxidative stress generated by free radical production. Heavy metals concentration can be decreased through various procedures including bioremediation, pyrolysis, phytoremediation, rhizofiltration, biochar, and thermal process. This review discusses few heavy metals, their toxicity mechanisms, and their health impacts on cattle with special emphasis on the kidneys.

show abstract

Hesperidin and hesperetin against heavy metal toxicity: Insight on the molecular mechanism of mitigation

Cited by 49 publications

References 187 publications

Hepatoprotective Mechanism of Apigenin via Suppression of Oxidative Inflammatory Signaling and Apoptosis against Hepatotoxicity Induced by CCl4 in Rats

Hepatoprotective Mechanism of Apigenin via Suppression of Oxidative Inflammatory Signaling and Apoptosis against Hepatotoxicity Induced by CCl4 in Rats

Resveratrol Mitigates Diabetic Testicular Dysfunction, Endocrine Deficits, and Insulin Resistance via Suppression of Sperm-Endocrine Aberrations and Oxidative Inflammation in Rats

A review of important heavy metals toxicity with special emphasis on nephrotoxicity and its management in cattle

Contact Info

Product

Resources

About