Oxidative stress and metallothionein expression in the liver of rats with severe thermal injury

Ding, Hui; Zhou, Bo; Liu, L.; Cheng, S.

doi:10.1016/s0305-4179(02)00018-9

Cited by 58 publications

(33 citation statements)

References 35 publications

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“…Thus, it seems that induction of NGAL in acute lung injury is related to generation of free radicals by DEP and LPS. Oxidative stress in cells is associated with an increased expression and activity of antioxidant enzymes (Ding et al 2002) and these defense systems are critical for ROS detoxification (Limón-Pacheco and Gonsebatt 2009). There are mounting evidence indicating that HO-1 gene expression is induced by stimulates that increase the cellular production of ROS, including heme, heavy metals, UV light, hydrogen peroxide, and lipopolysaccharide (Immenschuh and Ramadori 2000, Hayashi et al 2001, Bussolati et al 2004, Kikuchi et al 2005, Bach 2006).…”

Section: Discussionmentioning

confidence: 99%

Neutrophil Gelatinase-Associated Lipocalin induces the expression of heme oxygenase-1 and superoxide dismutase 1, 2

Bahmani

Halabian

Rouhbakhsh

et al. 2010

Cell Stress and Chaperones

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Lipocalin-2 (Lcn2, NGAL) is a member of the lipocalin super family with diverse function such as the induction of apoptosis, the suppression of bacterial growth, and modulation of inflammatory response. Much interest has recently been focused on the physiological/pathological role of the lipocalin-2 that is considered to be a novel protective factor against oxidative stress. However, its precise biological roles in this protection are not fully understood. In this report we intended to test the effect of lipocalin-2 on the expression of heme oxygenase (1, 2) and superoxide dismutase (1, 2) which are two strong antioxidants. NGAL was cloned to pcDNA3.1 plasmid by using genetic engineering method. The recombinant vector was transfected to CHO and HEK293T to establish stable cell expressing NGAL and the expression of HO-1, 2 and SOD 1, 2 were compared with appropriate controls by RT-PCR and western blot. On the other hand, expression of NGAL was suppressed by siRNA transfection in order to study the effect of lipocalin-2 on mentioned genes/proteins. The results showed that the expression of HO-1 and SOD 1, 2 enzymes were higher in cells expressing recombinant lipocalin-2 compared with the control cells. Although the expression of HO-1 was lower in NGAL silencing cells, the expression of SOD 1 and SOD 2 were higher. Our data suggest that NGAL is a potent inducer of HO-1 and somewhat SOD 1 and SOD 2 and it appears that part of antioxidant property of NGAL could be attributed to the induction of HO-1and SOD 1, 2 .

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Section: Discussionmentioning

confidence: 99%

Neutrophil Gelatinase-Associated Lipocalin induces the expression of heme oxygenase-1 and superoxide dismutase 1, 2

Bahmani

Halabian

Rouhbakhsh

et al. 2010

Cell Stress and Chaperones

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“…This is related to increased expression of Zn-binding proteins, such as metallothionein (MT)-I, with increased Zn content found in selected tissues (e. g., liver) at the expense of the plasma compartment [111,112]. This redistribution of Zn and expression of MT-I may play an important pathophysiologic role regarding antioxidant defenses and protein synthesis [113][114][115].…”

Section: Micronutrient Deficiencies and Oxidative Stress In Aldosteromentioning

confidence: 99%

Macro- and micronutrients in African-Americans with heart failure

et al. 2006

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An emerging body of evidence suggests secondary hyperparathyroidism (SHPT) may be an important covariant of congestive heart failure (CHF), especially in African-Americans (AA) where hypovitaminosis D is prevalent given that melanin, a natural sunscreen, mandates prolonged exposure of skin to sunlight and where a housebound lifestyle imposed by symptomatic CHF limits outdoor activities and hence sunlight exposure. In addition to the role of hypovitaminosis D in contributing to SHPT is the increased urinary and fecal losses of macronutrients Ca(2+) and Mg(2+) associated with the aldosteronism of CHF and their heightened urinary losses with furosemide treatment of CHF. Thus, a precarious Ca(2+) balance seen with reduced serum 25(OH)D is further compromised when AA develop CHF with circulating RAAS activation and are then treated with a loop diuretic. SHPT accounts for a paradoxical Ca(2+) overloading of diverse tissues and the induction of oxidative stress at these sites which spills over to the systemic circulation. In addition to SHPT, hypozincemia and hyposelenemia have been found in AA with compensated and decompensated heart failure and where an insufficiency of these micronutrients may have its origins in inadequate dietary intake, altered rates of absorption or excretion and/or tissue redistribution, and treatment with an ACE inhibitor or AT(1) receptor antagonist. Zn and Se deficiencies, which compromise the activity of several endogenous antioxidant defenses, could prove contributory to the severity of heart failure and its progressive nature. These findings call into question the need for nutriceutical treatment of heart failure and which is complementary to today's pharmaceuticals, especially in AA.

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“…ROS are first generated from the burned skin (26). Activated mononuclear phagocytes (27) and neutrophils (28,29) sequestered in systemic organs would also be the source of ROS.…”

Section: Discussionmentioning

confidence: 99%

The effect of silymarin on the liver in thermal burn injury

Yemişen¹

2014

mpj

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Oxidative stress and metallothionein expression in the liver of rats with severe thermal injury

Cited by 58 publications

References 35 publications

Neutrophil Gelatinase-Associated Lipocalin induces the expression of heme oxygenase-1 and superoxide dismutase 1, 2

Neutrophil Gelatinase-Associated Lipocalin induces the expression of heme oxygenase-1 and superoxide dismutase 1, 2

Macro- and micronutrients in African-Americans with heart failure

The effect of silymarin on the liver in thermal burn injury

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