# The Role of Selenium as an Antioxidant in the Treatment of Renal Cell Carcinoma

## TL;DR

This study examines how selenium affects kidney cancer cells by influencing oxidative stress and cell survival.

## Contribution

The study reveals selenium's dual role in modulating ROS and cell viability in renal cell carcinoma under different conditions.

## Key findings

- Selenium reduced ROS and increased cell viability when used alone.
- Selenium increased ROS and decreased cell viability when combined with oxidative stress.
- Cell viability was inversely related to ROS levels in treated groups.

## Abstract

Background: Antioxidants are said to have a major role in preventing cancerous growth, and selenium, being one of the vital trace elements, plays a crucial role in the oxidation-reduction system. Selenium, however, demonstrates a well-recognised dose- and context-dependent dual behaviour: while acting as an antioxidant at physiological levels, it may exert pro-oxidant and cytotoxic effects at higher concentrations, a phenomenon previously described in cancer biology. In parallel, reactive oxygen species (ROS), intracellular oxidants such as hydrogen peroxide, are key mediators of oxidative stress that influence cancer cell survival and death. Given this interplay, the role of selenium in modulating oxidative stress remains controversial.

Aim: To explore the effects of selenium as an antioxidant on renal cell carcinoma (RCC).

Methods: RCC cell lines under strict culture conditions were divided into two groups: control (group A) and experimental groups. Experimental groups were selenium treated (group B), exposed to oxidative stress induced with H₂O₂ (group C), and exposed to oxidative stress induced with H₂O₂ followed by selenium treatment (group D) and selenium treatment followed by oxidative stress induced by H₂O₂ (group E). Cell growth and survival were evaluated in each group after 72 hours. Evaluation of the ROS was done using the Cellular Reactive Oxygen Species Detection Assay Kit (Abcam; ab186029), and cell viability was measured using MTT reagent (Sigma; 11465007001).

Results: The generation of the ROS was significantly high in groups C (125.4% ± 14.6), D (132.9% ± 16.6), and E (135.3% ± 22.1) when compared to groups A (100% ± 14) and B (91.7% ± 14.6). Moreover, the RCC cell viability was 98.7% ± 10.8 in group B compared to C, D and E (80.8% ± 5.4, 79.7% ± 5.9 and 74.8% ± 8.8, respectively). Moreover, an association was observed between the viability of cells and ROS generation. The higher the ROS generation (groups C, D, and E), the lower its viability. Likewise, the lower the ROS generation (group B), the more viable were the cells.

Conclusions: the effects of selenium as an antioxidant in promoting cell viability in renal cell carcinoma have been controversial. In some aspects, it reduced ROS production, which increased cancer cell viability. While in another setting, selenium increased ROS levels, which correlated with more cell death. Therefore, further research needs to be conducted to prove the true effects of selenium on cancer cells.