Severe Vitamin E deficiency exacerbates acute hyperoxic lung injury associated with increased oxidative stress and inflammation

2008 ◽  
Vol 42 (6) ◽  
pp. 602-612 ◽  
Author(s):  
Shigeo Yamaoka ◽  
Han-Suk Kim ◽  
Tohru Ogihara ◽  
Shinya Oue ◽  
Kimitaka Takitani ◽  
...  
1999 ◽  
Vol 822 (1-2) ◽  
pp. 80-87 ◽  
Author(s):  
Richard P. Copp ◽  
Thomas Wisniewski ◽  
Fayçal Hentati ◽  
Abdelmajid Larnaout ◽  
Mongi Ben Hamida ◽  
...  

1999 ◽  
Vol 277 (6) ◽  
pp. L1214-L1223 ◽  
Author(s):  
Funmei Yang ◽  
Jacqueline J. Coalson ◽  
Heather H. Bobb ◽  
Jacqueline D. Carter ◽  
Jameela Banu ◽  
...  

Oxidative stress plays a central role in the pathogenesis of acute and chronic pulmonary diseases. Safe sequestration of iron, which participates in the formation of the hydroxyl radical, is crucial in the lung's defense. We used a mouse line defective in the major iron transport protein transferrin to investigate the effect of aberrant iron metabolism on the lung's defense against oxidative injury. The tolerance to hyperoxic lung injury was greater in the hypotransferrinemic than in wild-type mice as documented by histopathology and biochemical indexes for lung damage. There was no increase in the levels of intracellular antioxidants, inflammatory cytokines, and heme oxygenase-1 in the hypotransferrinemic mouse lung compared with those in wild-type mice. However, there were elevated expressions of ferritin and lactoferrin in the lung of hypotransferrinemic mice, especially in the alveolar macrophages. Our results suggest that pulmonary lactoferrin and ferritin protect animals against oxidative stress, most likely via their capacity to sequester iron, and that alveolar macrophages are the key participants in iron detoxification in the lower respiratory tract.


2014 ◽  
Vol 54 (6) ◽  
pp. 694 ◽  
Author(s):  
Shimin Liu ◽  
David Masters ◽  
Mark Ferguson ◽  
Andrew Thompson

Vitamin E concentrations in dried pastures, stubble and most grains are below the recommended requirement of 10–25 mg/kg dry matter (DM). Sheep grazing in an environment when dry pastures and cereal crop stubbles are their primary source of nutrients for a few months have a high risk of developing vitamin E deficiency. If the low vitamin E status coincides with late gestation, the neonate is likely to have a deficiency of vitamin E. Some of the consequences of this are well known, with nutritional myopathy (with high mortality) a risk in young growing sheep unless vitamin E supplements are provided. Vitamin E plays an important role in the management of oxidative stress. Sperm are subject to oxidative damage due to high metabolic rate and high concentration of polyunsaturated fatty acids in their membranes. Oxidative stress may also compromise follicular development and ovarian activity. Vitamin E is also involved with improvement in immune response. For these reasons, vitamin E status is important for reproductive efficiency in both males and females and in the survival of lambs and weaners. In addition, vitamin E deficiency is potentially exacerbated by a lack of other nutrients involved in the management of oxidative stress and immune function, such as selenium (Se) and sulfur amino acids. A Se concentration of 0.1 mg/kg DM in feedstuffs is required to maintain immune competency in sheep. In considering possible consequences for reproduction, further investigation is justified into: (i) effects of low vitamin E, in combination with low levels of other natural antioxidants, on the quality and quantity of sperm produced before and during mating; (ii) follicle development, fertilisation and embryonic mortality in Se-supplemented ewes; (iii) assessment of supplementing formulated antioxidants to rams and ewes during the mating season; (iv) managing oxidative stress in the newborn – consequences of large doses of vitamin E to ewes before parturition to boost lamb reserves; (v) potential benefits to lamb survival through boosting maternal innate immunity; (vi) choices for boosting antioxidant and immune function in ewes and lambs through ‘immune pack’ nutrient options that may target nutrients lacking in dry grass pastures; (vii) the potential role of heat stress in modifying the requirements for, and responses to, vitamin E in extensive grazing systems.


Nutrition ◽  
2019 ◽  
Vol 63-64 ◽  
pp. 57-60 ◽  
Author(s):  
Elisa Trotta ◽  
Stefano Bortolotti ◽  
Gabriella Fugazzotto ◽  
Cinzia Gellera ◽  
Sara Montagnese ◽  
...  

1998 ◽  
Vol 274 (4) ◽  
pp. L582-L590 ◽  
Author(s):  
Jennifer L. Taylor ◽  
Martha Sue Carraway ◽  
Claude A. Piantadosi

Heme oxygenase (HO)-1, which catalyzes heme breakdown, is induced by oxidative stress and may protect against oxidative injury. We hypothesized that induction of HO-1 by hemoglobin (Hb) in the lung would protect the rat from pulmonary O2 toxicity. Rats given intratracheal (IT) Hb showed lung-specific induction of HO-1 by 8 h by Western analysis. Rats were then pretreated for 8 h before 60 h of exposure to 100% O2 with either IT normal saline, Hb, or Hb plus the HO-1 inhibitor tin-protoporphyrin (SnPP). Both the Hb+O2 and Hb+O2+ SnPP animals had less lung injury than normal saline controls as indicated by lower pleural fluid volumes and wet-to-dry weight ratios ( P < 0.01). The improvement in injury in the two Hb-treated groups was the same despite a 61% decrease in HO enzyme activity in the Hb+SnPP group after 60 h of O2. In addition, inhibition of HO activity with SnPP alone before O2exposure did not augment the extent of hyperoxic lung injury. These results demonstrate that IT Hb induces lung HO-1 in the rat and protects against hyperoxia; however, the protection is not mediated by increased HO enzyme activity.


QJM ◽  
2019 ◽  
Vol 112 (12) ◽  
pp. 914-924 ◽  
Author(s):  
Y Fang ◽  
F Gao ◽  
Z Liu

Summary Objective To investigate the role of angiotensin-converting enzyme 2 (ACE2) in hyperoxic lung injury. Methods Adult mice were exposed to 95% O2 for 72 h to induce hyperoxic lung injury, and simultaneously treated with ACE2 agonist diminazene aceturate (DIZE) or inhibitor MLN-4760. ACE2 expression/activity in lung tissue and angiotensin (Ang)-(1–7)/Ang II in bronchoalveolar lavage fluid (BALF), and the severity of hyperoxic lung injury were evaluated. The levels of inflammatory factors in BALF and lung tissue and the expression levels of phospho-p65, p65 and IkBα were measured. Oxidative parameter and antioxidant enzyme levels in lung tissue were measured to assess oxidative stress. Finally, the expression levels of nuclear factor-erythroid-2-related factor (Nrf2), NAD(P)H quinine oxidoreductase 1 (NQO1) and heme oxygenase-1 (HO-1) were measured using Western blotting. Results Hyperoxia treatment significantly decreased lung ACE2 expression/activity and increased the Ang II/Ang-(1–7) ratio, while co-treatment with hyperoxia and DIZE significantly increased lung ACE2 expression/activity and decreased the Ang II/Ang-(1–7) ratio. By contrast, co-treatment with hyperoxia and MLN-4760 significantly decreased lung ACE2 expression/activity and increased the Ang II/Ang-(1–7) ratio. Hyperoxia treatment induced significant lung injury, inflammatory response and oxidative stress, which were attenuated by DIZE but aggravated by MLN-4760. The NF-κB pathways were activated by hyperoxia and MLN-4760 but inhibited by DIZE. The Nrf2 pathway and its downstream proteins NQO1 and HO-1 were activated by DIZE but inhibited by MLN-4760. Conclusion Activation of ACE2 can reduce the severity of hyperoxic lung injury by inhibiting inflammatory response and oxidative stress. ACE2 can inhibit the NF-κB pathway and activate the Nrf2/HO-1/NQO1 pathway, which may be involved in the underlying mechanism.


PEDIATRICS ◽  
1958 ◽  
Vol 22 (3) ◽  
pp. 494-506
Author(s):  
William A. Blanc ◽  
Joseph D. Reid ◽  
Dorothy H. Andersen

Ceroid-pigment is present in the smooth muscle fibers of the gastrointestinal tract of patients with cystic fibrosis of the pancreas. It is first seen during the second year of life. It is found in all patients of 5 years of age and older, and the amount increases with age. It has not been found in other pediatric conditions with the exception of biliary atresia and cirrhosis of the liver. Extensive ceroid deposit probably represents an expression of prolonged and severe vitamin-E deficiency, related to protracted malabsorption of fat-soluble tocopherols. Alterations of striated muscle appear to be rare and minimal in cystic fibrosis of the pancreas.


1995 ◽  
Vol 18 (3) ◽  
pp. 537-542 ◽  
Author(s):  
Brooks M. Hybertson ◽  
Jonathan A. Leff ◽  
Connie J. Beehler ◽  
Patrick C. Barry ◽  
John E. Repine

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