Secondary reactive oxygen species production after PDT during pulmonary tumor growth in sera of nude mice

Pulmonary metastases of the A549-derived lung adenocarcinoma tumors growing in nude mice. A multiple case study.

“…Although the growth of tumors undergoing PDT Ph was inhibited in comparison to untreated control tumors (not shown), the therapeutic protocol using 1 mg/kg of Photofrin ® and 655 nm red light cannot be considered as being safe for the treated animals due to the appearance of numerous metastases in lungs causing a high risk of severe respiratory problems (Douillard et al, 2013). Such dose of the drug is reported as "low" (Peng et al, 2001) in comparison with the clinically approved dose of 2 mg/kg in PDT of lung cancer (Moghissi, 2008).…”

Involvement of retinoblastoma-associated protein 48 during photodynamic therapy of cervical cancer cells

“…Cancer is defined as abnormal cell growth characterized by increased cell proliferation and decreased apoptosis. With exposure to PDT, cells initiate complex responses, including the formation of highly reactive singlet oxygen or other free radicals like hydrogen peroxides or superoxide anions, which can kill tumor cells directly by apoptosis and/or necrosis (10,23). The finding that PDT may cause an apoptotic response in target cells without complete disruption of the tissue has provided an explanation for the ideal characteristics required of any ablative technology for focally treating early cervical cancer.…”

Influence of Vitamins on Secondary Reactive Oxygen Species Production in Sera of Patients with Resectable NSCLC

“…Global antioxidant measurements may be more physiologically relevant because they take account of potential synergistic or antagonistic [24] effects of antioxidants that can be very different in nature: vitamins, albumin, enzymes, more specific molecules such as glutathione, but also non-specific compounds with antioxidant properties such as uric acid or bilirubin. In addition, oxidative stress following a metabolic impairment does not evolve linearly as during cancer growth [10] and therefore antioxidants should not be given blindly whatever the time of administration. What is said to be an antioxidant in a healthy person could be a strong pro-oxidant in other circumstances and induce deleterious effects during certain periods of time.…”

“…In addition to ROS, singlet oxygen ( 1 O 2 )—a molecular excited form of oxygen that is generated during inflammatory reactions or during photoreactions [5,6]—can undergo de-activation to produce secondary ROS as hydroxyls, alkoxyls, peroxyls, superoxide anion, and peroxides (SOS), and is strongly oxidant for many biological targets, either directly or through the formation of SOS [7,8]. We demonstrated that resistance to SOS was decreased in advanced cancers—experimentally and in patients [9,10]—and recently, a correlation between antioxidant, Vitamins (Vit) and inflammation biomarkers had been observed in patients with metabolic syndrome [11], something that could to some extent influence cancer growth. Whereas several studies aimed at reinforcing antioxidant defense during diseases or deficiencies, using vitamins has shown a positive effect.…”