Arabic Gum Could Alleviate the Aflatoxin B1-provoked Hepatic Injury in Rat: The Involvement of Oxidative Stress, Inflammatory, and Apoptotic Pathways

Abstract

Aflatoxin B1 (AF) is an unavoidable environmental pollutant that contaminates food, feed, and grains, which seriously threatens human and animal health. Arabic gum (AG) has recently evoked much attention owing to its promising therapeutic potential. Thus, the current study was conducted to look into the possible mechanisms beyond the ameliorative activity of AG against AF-inflicted hepatic injury. Male Wistar rats were assigned into four groups: Control, AG (7.5 g/kg b.w/day, orally), AF (200 µg/kg b.w), and AG plus AF group. AF induced marked liver damage expounded by considerable changes in biochemical profile and histological architecture. The oxidative stress stimulated by AF boosted the production of plasma malondialdehyde (MDA) level along with decreases in the total antioxidant capacity (TAC) level and glutathione peroxidase (GPx) activity. Additionally, AF exposure was associated with down-regulation of the nuclear factor erythroid2–related factor2 (Nrf2) and superoxide dismutase1 (SOD1) protein expression in liver tissue. Apoptotic cascade has also been evoked following AF-exposure, as depicted in overexpression of cytochrome c (Cyto c), cleaved Caspase3 (Cl. Casp3), along with enhanced up-regulation of inflammatory mediators such as tumor necrosis factor-α (TNF-α), interleukin (IL)-6, inducible nitric oxide synthase (iNOS), and nuclear factor kappa-B transcription factor/p65 (NF-κB/p65) mRNA expression levels. Interestingly, the antioxidant and anti-inflammatory contents of AG may reverse the induced oxidative damage, inflammation, and apoptosis in AF-exposed animals.

Gum acacia dietary fiber: Significance in immunomodulation, inflammatory diseases, and cancer

“…Pro‐inflammatory cytokines such as IL‐6, TNF‐alpha, iNOS, and NF‐kappaB/p65, which had increased in liver tissue due to AF exposure, exhibited significant reductions when GA was administered concurrently with AF. Moreover, the protein levels of Nrf2, which had significantly decreased in liver tissue following AF exposure, were restored in the group of rats simultaneously treated with GA and AF (Ahmed, El‐Rayes, et al, 2022).…”

Therapeutic Effect of Natural Products and Dietary Supplements on Aflatoxin-Induced Nephropathy

“…Aflatoxins are classified into six groups: B1, B2, G1, G2, M1 and M2, according to their fluorescence and chromatographic properties [ 34 , 35 , 36 ]. Aflatoxins are listed as aflatoxin B1 (AFB1) > aflatoxin G1 > aflatoxin B2 > aflatoxin G2 according to the strength of their toxic effects [ 37 ].…”

“…Natural remedies offer multiple pathways, diverse targets, and minimal toxicity, leading to increased research into their use in the prevention and treatment of kidney disease [ 69 ]. The literature suggests that natural remedies may reduce AFB1-induced toxicity by increasing antioxidant and anti-inflammatory capabilities and modulating gene expression of detoxifying enzymes, thereby limiting toxicity and tissue damage [ 16 , 20 , 34 , 47 ]. Dietary antioxidants derived from medicinal plants play an important role in the treatment of various diseases by boosting the body’s intrinsic antioxidant system.…”

Microalgae (Chlorella vulgaris) attenuates aflatoxin-associated renal injury

“…The Food and Drug Administration (FDA) has classified AFTs as ineluctable contaminants due to their pervasiveness along with their potential jeopardy to the health of humans and animals ( Abdel-Daim et al, 2021 ). AFT intoxication has genotoxic, mutagenic, and carcinogenic impacts and is designated by the International Agency for Research as a class-I carcinogen in various organs ( Hebels et al, 2009 ; Ahmed et al, 2022 ).…”

“…Thereafter, AFTO is detoxified by the phase-II glutathione (GSH) system to a minimally toxic GSH complex, which is then excreted from the cells via the mercapturic acid pathway ( Dlamini et al, 2021 ). It is intriguing that in addition to the liver ( Ahmed et al, 2022 ), the kidney is a probable target since AFT and AFTO are preferentially absorbed and concentrated by tubular cells, and their accumulation in the renal medulla before being expelled in the urine causes direct renal tubular damage ( Wang et al, 2022 ).…”