Protective effects of chlorogenic acid, curcumin and β-carotene against γ-radiation-induced in vivo chromosomal damage

1993 ◽  
Vol 303 (3) ◽  
pp. 109-112 ◽  
Author(s):  
Suresh K. Abraham ◽  
Lakshmi Sarma ◽  
P.C. Kesavan
Keyword(s):  
Chlorogenic Acid ◽  
Protective Effects ◽  
Chromosomal Damage ◽  
Γ Radiation ◽  
Radiation Induced ◽  
Β Carotene

scholarly journals The Zebrafish Embryo as a Model to Test Protective Effects of Food Antioxidant Compounds

Molecules ◽  
2021 ◽  
Vol 26 (19) ◽  
pp. 5786
Author(s):  
Cristina Arteaga ◽  
Nuria Boix ◽  
Elisabet Teixido ◽  
Fernanda Marizande ◽  
Santiago Cadena ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Zebrafish Embryo ◽  
In Vitro Assays ◽  
Antioxidant Compounds ◽  
Protective Effects ◽  
Tert Butyl Hydroperoxide ◽  
In Vivo Effects ◽  
Β Carotene

The antioxidant activity of food compounds is one of the properties generating the most interest, due to its health benefits and correlation with the prevention of chronic disease. This activity is usually measured using in vitro assays, which cannot predict in vivo effects or mechanisms of action. The objective of this study was to evaluate the in vivo protective effects of six phenolic compounds (naringenin, apigenin, rutin, oleuropein, chlorogenic acid, and curcumin) and three carotenoids (lycopene B, β-carotene, and astaxanthin) naturally present in foods using a zebrafish embryo model. The zebrafish embryo was pretreated with each of the nine antioxidant compounds and then exposed to tert-butyl hydroperoxide (tBOOH), a known inducer of oxidative stress in zebrafish. Significant differences were determined by comparing the concentration-response of the tBOOH induced lethality and dysmorphogenesis against the pretreated embryos with the antioxidant compounds. A protective effect of each compound, except β-carotene, against oxidative-stress-induced lethality was found. Furthermore, apigenin, rutin, and curcumin also showed protective effects against dysmorphogenesis. On the other hand, β-carotene exhibited increased lethality and dysmorphogenesis compared to the tBOOH treatment alone.

Protective effects of tetrahydropalmatine against γ-radiation induced damage to human endothelial cells

Life Sciences ◽  
2010 ◽  
Vol 87 (1-2) ◽  
pp. 55-63 ◽  
Author(s):  
Jing Yu ◽  
Bin-kui Piao ◽  
Ying-xia Pei ◽  
Xin Qi ◽  
Bao-jin Hua
Keyword(s):  
Endothelial Cells ◽  
Protective Effects ◽  
Human Endothelial Cells ◽  
Γ Radiation ◽  
Radiation Induced

scholarly journals Sphingolipids as a Novel Therapeutic Target in Radiation-Induced Lung Injury

2021 ◽  
Author(s):  
Jeffrey R. Jacobson
Keyword(s):  
Lung Injury ◽  
Cell Injury ◽  
Inflammatory Responses ◽  
Small Animal ◽  
Protective Effects ◽  
Sphingosine 1 Phosphate ◽  
Radiation Induced ◽  
Injury Models

AbstractRadiation-induced lung injury (RILI) is a potential complication of thoracic radiotherapy that can result in pneumonitis or pulmonary fibrosis and is associated with significant morbidity and mortality. The pathobiology of RILI is complex and includes the generation of free radicals and DNA damage that precipitate oxidative stress, endothelial cell (EC), and epithelial cell injury and inflammation. While the cellular events involved continue to be elucidated and characterized, targeted and effective therapies for RILI remain elusive. Sphingolipids are known to mediate EC function including many of the cell signaling events associated with the elaboration of RILI. Sphingosine-1-phosphate (S1P) and S1P analogs enhance EC barrier function in vitro and have demonstrated significant protective effects in vivo in a variety of acute lung injury models including RILI. Similarly, statin drugs that have pleiotropic effects that include upregulation of EC S1P receptor 1 (S1PR1) have been found to be strongly protective in a small animal RILI model. Thus, targeting of EC sphingosine signaling, either directly or indirectly, to augment EC function and thereby attenuate EC permeability and inflammatory responses, represents a novel and promising therapeutic strategy for the prevention or treatment of RILI.

scholarly journals Protective effects of caffeic acid phenethyl ester on radiation induced lung injury in rats

2008 ◽  
Vol 31 (5) ◽  
pp. 242 ◽  
Author(s):  
Oguz Galip Yildiz ◽  
Serdar Soyuer ◽  
Recep Saraymen ◽  
Celalettin Eroglu
Keyword(s):  
Radiation Therapy ◽  
Lung Injury ◽  
Caffeic Acid ◽  
Radiation Treatment ◽  
Caffeic Acid Phenethyl Ester ◽  
Albino Rats ◽  
Protective Effects ◽  
Sod Activity ◽  
Radiation Induced

Purpose: The prevention of radiation-induced pulmonary toxicity may help to improve radiation therapy in the cancer patient. The aim of this study was to investigate the pulmonary protective effects of caffeic acid phenethyl ester (CAPE), an antioxidant, on radiation-induced lung injury in rats. Methods:30 Wistar albino rats were divided into three groups and treated with saline, Radiation (RT) and RT + CAPE respectively. All rats were treated with CAPE (50 ?mol/kg i.p.) or saline. The first dose of CAPE was injected 24 h before radiation and application continued daily, with radiation in second day and 2 days more after the radiation treatment. Radiation dose was 800 cGy for total body. At 72 hr after the last radiation application, under general anesthesia using ip ketamine, the lungs were removed immediately after decapitation. After sacrification, antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) activities and malondiadehyde (MDA) levels were evaluated in lung tissue. Results: The level of malondialdehyde (MDA) was higher in the RT group (233.4±1.5 nmol/g protein) than in both the control (131.8±0.92) and the RT + CAPE (151.4±1.8) groups (P < 0.001). However, CAT activity was decreased in the RT group (7.26±0.27 Umg protein) compared with control (8.49±0.51) and increased again in the RT + CAPE group (8.31±0.56; P < 0.001). In accord with CAT activity, SOD activity in the RT group (0.42±0.07 nmolMDA/g wet tissue) was different from the control (0.78±0.02) and RT + CAPE (0.86±0.06) groups (P < 0.001). Conclusion: CAPE aplication with radiation therapy attenuated radiation induced pulmonary injury in vivo, possibly by its antioxidant effect.

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