“…In vivo, NO release after PVC-MuLV infection could be inferred by 3-NT immunoreactivity. Although NO release can also have immune (Babior 1999) and neuroprotective effects (Wink et al, 1996), the fact that vacuolation, gliosis, and eventual neuronal death followed the appearance of 3-NT immunoreactivity suggests that free radical injury may be the predominant effect in this infection.…”
Vacuolation in cellular organelles within the central nervous system is a common manifestation of oxidative injury. We found that the spongiform vacuolation observed in PVC‐211 murine leukemia virus (PVC‐MuLV) neurodegeneration was associated with oxidative damage as detected by immunoreactivity for 3‐nitrotyrosine and protein carbonyl groups. This oxidative injury was present in brain before or concomitant with the appearance of activated microglia, vacuolation, and gliosis that characterize PVC‐MuLV neuropathology. Treatment of infected F344 rat pups with the antioxidant vitamin E transiently protected and prolonged the latency of PVC‐MuLV neurodegeneration. Taken together, these findings implicate oxidative damage and lipid peroxidation in the pathogenesis of PVC‐MuLV neurodegeneration. This animal model may be useful for studies of mechanisms and potential therapies for progressive neurodegeneration following a well‐defined insult. J. Neurosci. Res. 62:440–450, 2000. Published 2000 Wiley‐Liss, Inc.
“…In vivo, NO release after PVC-MuLV infection could be inferred by 3-NT immunoreactivity. Although NO release can also have immune (Babior 1999) and neuroprotective effects (Wink et al, 1996), the fact that vacuolation, gliosis, and eventual neuronal death followed the appearance of 3-NT immunoreactivity suggests that free radical injury may be the predominant effect in this infection.…”
Vacuolation in cellular organelles within the central nervous system is a common manifestation of oxidative injury. We found that the spongiform vacuolation observed in PVC‐211 murine leukemia virus (PVC‐MuLV) neurodegeneration was associated with oxidative damage as detected by immunoreactivity for 3‐nitrotyrosine and protein carbonyl groups. This oxidative injury was present in brain before or concomitant with the appearance of activated microglia, vacuolation, and gliosis that characterize PVC‐MuLV neuropathology. Treatment of infected F344 rat pups with the antioxidant vitamin E transiently protected and prolonged the latency of PVC‐MuLV neurodegeneration. Taken together, these findings implicate oxidative damage and lipid peroxidation in the pathogenesis of PVC‐MuLV neurodegeneration. This animal model may be useful for studies of mechanisms and potential therapies for progressive neurodegeneration following a well‐defined insult. J. Neurosci. Res. 62:440–450, 2000. Published 2000 Wiley‐Liss, Inc.
“…Evidence from various vertebrate and invertebrate models indicates that certain ROI and RNI, in particular d O 2 À , H 2 O 2 , and d NO, are not only cytotoxic molecules induced upon immune challenge, but also important cell-signaling molecules (Adler et al, 1999;Babior, 1999;Baeuerle et al, 1996;Bauer, 2002;Franchini et al, 1995;Stefano and Ottaviani, 2002). Elevated levels of one or more of these molecules have been identified in immune reactive Drosophila (Foley and O'farrell, 2003;Nappi and Vass, 2001), in Anopheles in response to Plasmodium infections (Dimopoulos et al, 2001(Dimopoulos et al, , 1998Dimopoulos, 2003;Fritsche et al, 2001;Kumar et al, 2003;Luckhart and Rosenberg, 1999;Luckhart et al, 1998), in trypanosome-infected Rhodnius prolixus (Whitten et al, 2001), and in immuneactivated lepidopteran hemocytes (Weiske and Wiesner, 1999).…”
Section: Interactions Of Melanin Intermediates With Roi and Rnimentioning
confidence: 99%
“…Depending on the species, innate immune effector responses may include phagocytosis, the synthesis of extracellular matrix, cell adhesion and pattern recognition molecules, reactive intermediates of oxygen (ROI) and nitrogen (RNI), proapoptotic molecules, pro-inflammatory cytokines, antimicrobial peptides, and molecules associated with iron sequestration and the maintenance of intracellular redox homeostasis ( Fig. 1) (Babior, 1999;Beutler, 2004;Blandin and Levashina, 2004;Bodian et al, 2004;Bulet et al, 2004;Cerenius and Soderhall, 2004;Dziarski, 2004;Ganz, 2003;Nappi and Vass, 2001;Ottaviani et al, 2004;Tunaz et al, 2003). The demonstration of striking parallels between the innate immune responses of insects and mammals has led some investigators to propose a common ancestry for these processes (Holland and Tolman, 1999;Janeway and Medzhitov, 2002;Ottaviani et al, 1995).…”
“…Indeed, several are more potent than mitochondria. The best studied of these is the NADPH (reduced form of NAD phosphate) oxidase of macrophages and CNS microglia (for review see [12]). Although the exquisitely regulated NADPH oxidase complex was initially thought to be confined exclusively to macrophages and microglia, NADPH oxidases have been implicated in growth factor signaling in a variety of cell types (see for example [13 -15]), including nerve cells [16].…”
Free radicals and reactive oxygen species cell death, the specific cellular changes can be quite different depending on the initial stimulus and the (ROS) are involved in a variety of different cellular type of cell involved. These data, along with the eviprocesses ranging from apoptosis and necrosis to cell dence that ROS can modify a number of intracellular proliferation and carcinogenesis. Cells contain multiple signaling pathways including protein phosphatases, sites for ROS production and a few mechanisms for protein kinases and transcription factors, suggest that their degradation. Which of these sites is activated by a given stimulus may play a role in dictating the subse-the majority of the effects of ROS on cells are quent downstream effects of the ROS generated on through their actions on signaling pathways rather cellular function. Even when the ultimate outcome is than via nonspecific damage of intracellular macrosimilar, such as when ROS production leads to molecules.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.