Role of Fucoxanthin towards Cadmium-induced renal impairment with the antioxidant and anti-lipid peroxide activities

Abstract

Kidney damages caused by cadmium are considered to be one of the most dangerous consequences for the human body. This study aimed to investigate the protective effects of fucoxanthin supplementation on mice models subjected to cadmium-induced kidney damage. The mice treated with cadmium chloride (CdCl 2 ) were observed to have significantly reduced the crosssection area of glomeruli. Cadmium exposure has also caused the damage of the structural integrity of mitochondria and increased blood urea nitrogen (BUN), kidney injury molecule 1 (KIM1), and neutrophil gelatinase associated lipocalin (NGAL) levels. Peroxidase (POD), superoxide dismutase (SOD), catalase (CAT), and ascorbate peroxidase (APX) levels in cadmium-exposed mice were markedly declined. Caspase3, caspase8, and caspase9 gene expressions in association with apoptosis were dramatically elevated in renal tissues. The CdCl 2 treated mice were orally administered with 50 mg/kg Shenfukang, 10 mg/kg, 25 mg/kg, and 50 mg/kg fucoxanthin for 14 days. The results revealed that high doses of fucoxanthin administration significantly decreased BUN, KIM1, NGAL levels, increasing POD, SOD, CAT, and ascorbate APX levels. Fucoxanthin administration also promoted recovery of the renal functions, micro-structural organization, and ultrastructural organization in the renal cells. In summary, the ameliorative effects of fucoxanthin supplementation against cadmium-induced kidney damage were mediated via inhibiting oxidative stress and apoptosis, promoting the recovery of structural integrity of mitochondria.

Comprehensive Molecular Study Reveals the Potential Role of Chebulinic Acid and Boeravinone B to Establish Redox Homeostasis in Metabolically Stressed Cells

“…3a). Earlier studies have showed the protective effects of fucoxanthin supplementation restored structural integrity of mitochondria in case of kidney damage caused by the Cadmiumexposed mice model [49]. In accordance with earlier reports, in our investigation stressed cells attained normal morphology and mitochondria functioning after CA and BB treatments.…”

A Systematic Review on Marine Algae-Derived Fucoxanthin: An Update of Pharmacological Insights

“…In TGFβ1-induced oxidative stress with excessive ROS accumulation in the human hepatic stellate cells model, primary metabolites of fucoxanthin such as fucoxanthinol and amarouciaxanthin A were treated in cells that showed preventive effects by antioxidant potentials by a reduced level of ROS and the increased expression of Nrf2 proteins [ 6 ]. In another study conducted by Yang and the team [ 8 ], the peroxidase, SOD, CAT, and ascorbate peroxidase in cadmium-exposed thyroid tissues in mice were decreased, and however, significantly recovered after fucoxanthin administration, through antioxidant activities together with downregulated ERK-mediated apoptosis pathways. Accumulating results suggest that fucoxanthin as an antioxidant with a multitude of protective functions in the in vitro and in vivo studies can be a lead compound for future translational research into clinical trials.…”

“…In the cadmium chloride-treated mice model, fucoxanthin protected the kidney by inhibiting oxidative stress and apoptosis, and recovering mitochondrial structural integrity. It significantly reduced apoptosis-related markers such as caspase-3 and caspase-9; and improved antioxidant activity by increasing the levels of SOD, CAT, and peroxidase (POD) [ 8 ].…”

“…Researchers are increasingly interested in the pharmacological importance of this naturally occurring fucoxanthin, alongside applications in the food and cosmeceutical industries [ 5 ]. Fucoxanthin has strong antioxidant potency, as evidenced by various cell culture models [ 6 , 7 ] and animal studies [ 8 , 9 ], potentially involved in regulating the Nrf2/ARE pathway. Yang and his colleague reported the anti-inflammatory effect of fucoxanthin [ 10 ], and their molecular mechanisms of prevention were characterized by the inhibition of NF-κB-related pathways [ 11 ].…”

Elucidation of Antioxidant and Neuroprotective Potential of Fucoxanthin Isolated from Brown Seaweed Sargassum oligocystum

“…Recent reports showed that fucoxanthin inhibits apoptosis and oxidative stress, and induces autophagy through Nrf2 (Pajares et al 2016). Moreover, PLGA-PEG (Poly lactide-co-glycolide (PLGA) with poly ethylene glycol (PEG)) nanoparticles containing fucoxanthin promoted the antioxidant activity by elevating superoxide dismutase (SOD), and catalase (CAT) in the brain (Yang et al 2021a). In addition, fucoxanthin has also been reported to indirectly activate Nrf2/ARE pathway via Akt (protein kinase B, PKB) pathways.…”