Reactive oxygen species and nitric oxide in viral diseases

Abstract

Metabolites derived from superoxide (02"-) and nitric oxide (NO.) play an important role in antimicrobial and antitumoral defense, but may also harm the host. Low levels of such metabolites can also facilitate viral replication because of their mitogenic effects on cells. Most viruses grow better in proliferating cells, and indeed, many viruses induce in their host cell changes similar to those seen early after treatment with mitogenic lectins. Influenza and paramyxoviruses activate in phagocytes the generation of superoxide by a mechanism involving the interaction between the viral surface glycoproteins and the phagocyte's plasma membrane. Interestingly, viruses that activate this host defense mechanism are toxic when injected in the bloodstream of animals. Mice infected with influenza virus undergo oxidative stress. In addition, a wide array of cytokines are formed in the lung, contributing to the systemic effects of influenza. Oxidative stress is seen also in chronic viral infections, such as AIDS and viral hepatitis. Oxidant production in viral hepatitis may contribute to the emergence of hepatocellular carcinoma, a tumor seen in patients after years of chronic inflammation of the liver. Antioxidants and agents that downregulate proinflammatory cytokines and lipid mediators may be a useful complement to specific antiviral drugs in the therapy of viral diseases.

Oxidative stress in cells infected with bovine viral diarrhoea virus: a crucial step in the induction of apoptosis.

“…Oxidative stress has been suggested to be a mediator of apoptosis induced by a variety of triggers, including virus infections (Buttke & Sandstrom, 1994 ;Schwarz, 1996 ;Peterhans, 1997). This was frequently shown either by the addition of ROS or by the anti-apoptotic effect of certain antioxidants.…”

“…Many of these signals are known to also induce oxidative stress (Buttke & Sandstrom, 1994). Evidence regarding the role of reactive oxygen species (ROS) in the replication and pathogenesis of human immunodeficiency virus has led to an increased interest in the role of oxidative stress in other virus infections (Peterhans, 1994 ;Schwarz, 1996 ;Israe$ l & Gougerot-Pocidalo, 1997 ;Peterhans, 1997). The killing of infected cells by apoptosis is one of the mechanisms of host defence against virus infections.…”

Age and Organ Dependent Spontaneous Generation of Nuclear 8-Hydroxydeoxyguanosine in Male Fischer 344 Rats

“…A unique gene has recently been identified to be involved in the suppression of multiple aging phenotypes Kuro-o et al, 1997;Matsumura et al, 1998). This gene, klotho, might be a candidate target of epigenetic influences due to nuclear oxidative stress because its expression is down-regulated under situations such as diabetes mellitus, chronic renal failure , and lipopolysaccharide-induced inflammation , in all of which oxidative stress plays a critical role (Finkel, 1999;Hasselwander and Young, 1998;Hogg, 1998;Peterhans, 1997;Singal et al, 1998). The mitochondrion is a major cellular source of ROS, and thus its components are immediate targets of oxidative stress.…”

“…However, the defense systems may be overcome, leading to the phenomenon known as "oxidative stress" (Ames et al, 1993;Anisimov, 1998;Harman, 1988). In recent years, this has become recognized or suggested as participating in the development of senescence, carcinogenesis, and a wide variety of diseases, either aging-dependent or independent (Ames et al, 1993;Ando et al, 1998;Anisimov, 1998;Busciglio et al, 1998;Facchinetti et al, 1998;Feher et al, 1998;Feig et al, 1994;Floyd, 1990;Harman, 1988;Hasselwander and Young, 1998;Hogg, 1998;Kaplowitz and Tsukamoto, 1996;Kasai, 1997;Minamoto et al, 1999;Peterhans, 1997;Reiter, 1998;Saugstad, 1998;Schenker and Montalvo, 1998;Singal et al, 1998;Stadtman and Berlett, 1998;Thomson et al, 1998;Zs-Nagy et al, 1988).…”

Effect of Quail Egg Pretreatment on the Lipid Profile and Histomorphology of the Liver of Acetaminophen-Induced Hepatotoxicity in Rats

“…Examination of plasma lipids and lipoprotein levels will be helpful to evaluate the extent of the hepatic damage. It is well known that plasma levels of cytokines, lipid peroxides and antioxidant status could be changed under acute hepatitis which may interfere with the lipid metabolism in vivo [18].…”