Phytochemical Sulforaphane (Dithiolthiones), the Best for the Prevention and Treatment of Lung Diseases

Scientists may have found a bioactive compound for the prevention and treatment of lung diseases with no side effects, according to studies.

Lung diseases are medical conditions, affecting the upper respiratory tract, trachea, bronchi, bronchioles, alveoli, pleura and pleural cavity, and the nerves and muscles of breathing.

People with lung diseases have breathing problems, preventing them to get enough oxygen for the body needs.

According to the statistic from the World Health Organization, respiratory diseases are leading causes of death and disability in the world. chronic obstructive pulmonary disease (COPD) and asthma are 2 of the most common respiratory disease in the world, affecting 65 million and 334 million people, respectively.

3 million people die from chronic obstructive pulmonary disease (COPD) each year, making it the third leading cause of death worldwide. And 14% of 334 million people suffer from asthma are children.

Long-term smoking is considered one of the leading risk factor of lung diseases. Other risk factors associated with the onset of lung diseases include radon, Asbestos, second-hand smoke, and air pollution.

Depending on the are of the respiratory system effect. Lung diseases can be classified to
* Lung disease affecting the airway include asthma and COPD.

*Lung diseases affecting the air sac include pneumonia and tuberculosis.

* Lung diseases affecting the interstitium include interstitial lung disease.

* Lung diseases affecting the blood vessel include pulmonary embolism (PE).

* Lung diseases affecting the pleura include pleural effusion.

* Lung affecting the chest wall include obesity


Dithiolthiones are phytochemicals in the class of Organosulfides, found abundantly in cruciferous vegetables, garden sorrel, horseradish, etc.

With an aim to find a natural compound for the treatment of lung diseases researchers examined the effects of sulforaphane (SF) in the protein Nuclear factor-like 2 (Nrf2) in mice from arsenic-induced toxicity.
Where Nuclear factor-like 2 has been found to protect the body against a broad spectrum of diseases induced by environmental exposure to harmful substances through its detoxed activity.

Selected mice were exposed to 2 weeks of arsenic-containing dust. At the end of 2 weeks, tested mice showed pathological alterations, oxidative DNA damage, and mild apoptotic cell death in the lung.


Pretreatment of sulforaphane activated the expression of Nrf2 only blocked the alternation caused by arsenic-containing dust but also restored all the damages induced by the substances.


Furthermore, SF-mediated activation of Nrf2 also alleviated inflammatory responses by modulating cytokine production, thus reducing the oxidative stress in the tested mice.

These results clearly suggested that dietary intervention which targets the Nrf2 activation may have a significant effect on the reduction of adverse health effects associated with arsenic exposure.


In the mouse model, activation of NRF2 protein was also found to regulate the rhythmic expression of antioxidant genes involved in glutathione redox homeostasis in the mouse lung.

Moreover, in vivo bleomycin-induced lung fibrosis model, pretreatment of SF restored the lung function by blocking the phenotype caused by bleomycin.


According to the observation of the lungs of the arrhythmic Clock(Δ19) mice, SF increased the levels of NRF2 and glutathione, the antioxidants enzymes produced by the host mice.


The results suggested that NRF2 activated by SF not only inhibited the oxidative damage but also protect the tested mice lung against fibrositis.


Dr. Pekovic-Vaughan V, the lead scientist, after taking into account co and confounders, said, "Our findings reveal a pivotal role for the circadian control of the NRF2/glutathione pathway in combating oxidative/fibrotic lung damage, which might prompt new chronotherapeutic strategies for the treatment of human lung diseases, including idiopathic pulmonary fibrosis".


However, in wildtype neonatal mice exposed to hyperoxia. SF also found to activated Nrf2 activation through induced expression of anti-oxidant genes but did not attenuate alveolar growth arrest caused by exposure to hyperoxia.

These discovery strong suggested that activation of activated Nrf2 may have a certain limit in protecting the lung and lung tissues against alveolar growth exposed to an excess supply of oxygen (O2) or higher than the normal partial pressure of oxygen.


Taken altogether, depending on the types of lung diseases, bioactive compound sulforaphane may be used for the prevention and combined with the primary therapy for the treatment of lung diseases with no side effects.


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Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bioscience, ISSN 0975-6299.

References
(1) Sulforaphane prevents pulmonary damage in response to inhaled arsenic by activating the Nrf2-defense response. by Zheng Y1, Tao S, Lian F, Chau BT, Chen J, Sun G, Fang D, Lantz RC, Zhang DD. (PubMed)
(2) Transcriptional responses of neonatal mouse lung to hyperoxia by Nrf2 status by McGrath-Morrow SA1, Lauer T, Collaco JM, Lopez A, Malhotra D, Alekseyev YO, Neptune E, Wise R, Biswal S.(PubMed)
(3) The circadian clock regulates rhythmic activation of the NRF2/glutathione-mediated antioxidant defense pathway to modulate pulmonary fibrosis by Pekovic-Vaughan V1, Gibbs J, Yoshitane H, Yang N, Pathiranage D, Guo B, Sagami A, Taguchi K, Bechtold D, Loudon A, Yamamoto M, Chan J, van der Horst GT, Fukada Y, Meng QJ.(PubMed)