Sulforaphane Impact on Reactive Oxygen Species (ROS) in Bladder Carcinoma

Sulforaphane (SFN) is a natural glucosinolate found in cruciferous vegetables that acts as a chemopreventive agent, but its mechanism of action is not clear. Due to antioxidative mechanisms being thought central in preventing cancer progression, SFN could play a role in oxidative processes. Since redox imbalance with increased levels of reactive oxygen species (ROS) is involved in the initiation and progression of bladder cancer, this mechanism might be involved when chemoresistance occurs. This review summarizes current understanding regarding the influence of SFN on ROS and ROS-related pathways and appraises a possible role of SFN in bladder cancer treatment.

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The differential role of reactive oxygen species in early and late stages of cancer

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00247.2017 ◽

2017 ◽

Vol 313 (6) ◽

pp. R646-R653 ◽

Cited By ~ 36

Author(s):

Mohamad Assi

Keyword(s):

Reactive Oxygen Species ◽

Tumor Cells ◽

Cancer Progression ◽

Reactive Oxygen ◽

Pentose Phosphate ◽

Oxygen Species ◽

Redox Biology ◽

Oxidative Damages ◽

Late Stages

The large doses of vitamins C and E and β-carotene used to reduce reactive oxygen species (ROS) production and oxidative damages in cancerous tissue have produced disappointing and contradictory results. This therapeutic conundrum was attributed to the double-faced role of ROS, notably, their ability to induce either proliferation or apoptosis of cancer cells. However, for a ROS-inhibitory approach to be effective, it must target ROS when they induce proliferation rather than apoptosis. On the basis of recent advances in redox biology, this review underlined a differential regulation of prooxidant and antioxidant system, respective to the stage of cancer. At early precancerous and neoplastic stages, antioxidant activity decreases and ROS appear to promote cancer initiation via inducing oxidative damage and base pair substitution mutations in prooncogenes and tumor suppressor genes, such as RAS and TP53, respectively. Whereas in late stages of cancer progression, tumor cells escape apoptosis by producing high levels of intracellular antioxidants, like NADPH and GSH, via the pentose phosphate pathway to buffer the excessive production of ROS and related intratumor oxidative injuries. Therefore, antioxidants should be prohibited in patients with advanced stages of cancer and/or undergoing anticancer therapies. Interestingly, the biochemical and biophysical properties of some polyphenols allow them to selectively recognize tumor cells. This characteristic was exploited to design and deliver nanoparticles coated with low doses of polyphenols and containing chemotherapeutic drugs into tumor-bearing animals. First results are encouraging, which may revolutionize the conventional use of antioxidants in cancer.

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Role of reactive oxygen species in cis-dichlorodiammineplatinum-induced cytotoxicity on bladder cancer cells

British Journal of Cancer ◽

10.1038/bjc.1997.363 ◽

1997 ◽

Vol 76 (2) ◽

pp. 206-210 ◽

Cited By ~ 127

Author(s):

A Miyajima ◽

J Nakashima ◽

K Yoshioka ◽

M Tachibana ◽

H Tazaki ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Bladder Cancer ◽

Cancer Cells ◽

Reactive Oxygen ◽

Oxygen Species ◽

Bladder Cancer Cells ◽

In Cis

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Free radicals, lipid peroxidation and sperm function

Reproduction Fertility and Development ◽

10.1071/rd9950659 ◽

1995 ◽

Vol 7 (4) ◽

pp. 659 ◽

Cited By ~ 393

Author(s):

RJ Aitken

Keyword(s):

Reactive Oxygen Species ◽

Lipid Peroxidation ◽

Reactive Oxygen ◽

Human Spermatozoa ◽

Sperm Function ◽

Oxygen Species ◽

Normal Sperm ◽

Oxidative Processes ◽

Mammalian Spermatozoa

The cellular generation of reactive oxygen species was first observed in mammalian spermatozoa in the late 1940s. The field then remained dormant for 30 years until Thaddeus Mann and Roy Jones published a series of landmark papers in the 1970s in which the importance of lipid peroxidation as a mechanism for damaging mammalian spermatozoa was first intimated. The subsequent demonstration that human spermatozoa produce reactive oxygen species and are susceptible to peroxidative damage has triggered intense interest in the role of oxidative stress in the aetiology of male infertility. Moreover, data have recently been obtained to indicate that, although excessive exposure to reactive oxygen species may be harmful to spermatozoa, in physiological amounts these molecules are of importance in the control of normal sperm function. This review considers the dualistic role of reactive oxygen species and sets out the current understanding of the importance of oxidative processes in both the physiology and the pathology of the human spermatozoon. Extra keywords: human spermatozoa, reactive oxygen species.

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