Antioxidants Delay Clinical Signs and Systemic Effects of ENU Induced Brain Tumors in Rats

Abstract

According to our previous study suggesting that antioxidant properties of phytochemicals in the diet decrease glioma aggressiveness, we used a SUVIMAX-like diet ("Supplementation en VItamines et Minéraux AntioXydants") (enriched with alpha-tocopherol, beta carotene, vitamin C, zinc, and sodium selenite), adapted to rats. The present results showed that each of the antioxidants inhibited growth of glioma cells in vitro. When used in combination for in vivo studies, we showed a highly significant delay in the clinical signs of the disease, but not a statistical significant difference in the incidence of glioma in an Ethyl-nitrosourea (ENU)-model. The SUVIMAX-like diet decreased candidate markers of tumoral aggressiveness and gliomagenesis progression. The mRNA expressions of 2 common markers in human glioma: Mn-SOD (Manganese Superoxide Dismutase) and IGFBP5 (insulin growth factor binding protein) were reduced in the tumors of rats fed the antioxidant diet. In addition, the transcripts of two markers linked to brain tumor proliferation, PDGFRb (platelet-derived growth factor receptor beta) and Ki-67, were also significantly decreased. On the whole, our results suggest a protective role for antioxidants to limit aggressiveness and to some extent, progression of gliomas, in a rat model.

Therapeutic Potential of Selenium in Glioblastoma

“…These patients were given either 1,000 µg inorganic Se in form of sodium selenite by infusion in physiological saline per day for 4-8 weeks (Pakdaman, 1998), or 150 µg organic Se in combination with 60 IU vitamin E for several weeks to 1 year (Philipov and Tzatchev, 1990). This was also demonstrated in rodent xenograft-glioma model (Hervouet et al, 2013;Yakubov, 2019). Se-excessive diet and intrathecal treatment of Se were associated with a prolonged survival and delayed neurological deficits compared to controls or dietary Se-deficient animals (Yakubov, 2019).…”

“…Se-excessive diet and intrathecal treatment of Se were associated with a prolonged survival and delayed neurological deficits compared to controls or dietary Se-deficient animals (Yakubov, 2019). Similarly, Hervouet et al (2013) reported a beneficial neurological effect of a diet mixture of α-tocopherol, β-carotene, Se, vitamin C, and zink. Remarkably, the invasive morphology of malignant cells and the tumor aggressiveness were decreased after treatment of Se in both xenograft models (Hervouet et al, 2013;Yakubov, 2019).…”

Antioxidant Supplementation during Glioma Therapy: Friend or Foe?

“…In 2013, Hervouet et al found that using SUVIMAX-like diet (supplementation en vitamins et minéraux antioxydants), which was enriched with beta carotene, alpha tocopherol, vitamin C, zinc, and sodium selenite, was delayed the clinical signs on ethyl-nitrosourea induced glioma rat model, but gliomagenesis occurred. This diet just decreased the tumor aggressiveness [52].…”

Bioinformatics Analyses Reveal the Prognostic Value and Biological Roles of SEPHS2 in Various Cancers

“… 13 , 14 Results from animal model studies have demonstrated that Se treatment reduced tumor invasiveness and improved clinical symptoms in patients with glioblastoma. 15 , 16 It was demonstrated that selenoprotein P (SELP, SELENOP), TXNRD, and selenoprotein F (SELENOF, SEP15) promoted tumor initiation and growth, invasion and metastasis by targeting tumor-associated signaling pathways. 17 Specific methylation of GPX3 has been shown to be a target for early prevention and treatment of clear cell renal cell carcinoma.…”