Roles of β-Glucans in Oxidative Stress and Cancer

Antioxidant, anti‐inflammatory and beneficial metabolic effects of botryosphaeran [(1→3)(1→6)‐β‐d‐glucan] are responsible for its anti‐tumour activity in experimental non‐obese and obese rats bearing Walker‐256 tumours

“…The endogenous antioxidant defence of the body represented by SOD, CAT, GST, GSH and ASA, acts in the restoration and protection against damage by ROS, decreasing the cytotoxic effects of ROS, and slowing the progression of cancer. 10,[37][38][39] In addition, several studies have demonstrated the antioxidant and protective properties of β-glucans mediated by their capacity to remove free radicals and inhibit lipid peroxidation. 9,10,[13][14][15] To our knowledge, however, no study has demonstrated in animals the antioxidant effect associated with the two pathologies, obesity and cancer.…”

“…10,[37][38][39] In addition, several studies have demonstrated the antioxidant and protective properties of β-glucans mediated by their capacity to remove free radicals and inhibit lipid peroxidation. 9,10,[13][14][15] To our knowledge, however, no study has demonstrated in animals the antioxidant effect associated with the two pathologies, obesity and cancer.…”

“…8 The non-enzymatic system includes GSH, various plant natural products (flavonoids, polyphenols, tocopherols, carotenoids, curcumin), vitamins A, C and E, and carbohydrate biopolymers that include the β-D-glucans. 8,9 Excess ROS presents harmful effects to cellular macromolecules, such as lipids, proteins, and nucleic acids, 8,10 leading to damage in all parts of the cell (nucleus, cytoplasm and membranes), as they act by promoting chromosomal abnormalities and damage to macromolecules. These harmful effects lead to the activation of different signalling pathways, such as PI3K/Akt/mTOR pathway, which contribute to cell proliferation, cell metabolism, and lessens apoptosis, thus leading to cancer development.…”

“…Excess ROS presents harmful effects to cellular macromolecules, such as lipids, proteins, and nucleic acids, 8,10 leading to damage in all parts of the cell (nucleus, cytoplasm and membranes), as they act by promoting chromosomal abnormalities and damage to macromolecules. These harmful effects lead to the activation of different signalling pathways, such as PI3K/Akt/mTOR pathway, which contribute to cell proliferation, cell metabolism, and lessens apoptosis, thus leading to cancer development 9‐12 . On the other hand, higher levels of ROS may contribute to cancer cell death, promoting apoptosis and necrosis, and thus an anti‐tumorigenic effect, which can be associated with the mechanism of action of several antineoplastic drugs 8,9 …”

“…These harmful effects lead to the activation of different signalling pathways, such as PI3K/Akt/mTOR pathway, which contribute to cell proliferation, cell metabolism, and lessens apoptosis, thus leading to cancer development. [9][10][11][12] On the other hand, higher levels of ROS may contribute to cancer cell death, promoting apoptosis and necrosis, and thus an anti-tumorigenic effect, which can be associated with the mechanism of action of several antineoplastic drugs. 8,9 Obesity, and tumour development itself, can generate several changes in an individual's body, affecting various tissues and organs, such as the liver, adipose tissue and kidneys.…”