Changes in Tissue Levels of Glutathione, Extent of Lipid Peroxidation, and Activity of Glutathione Peroxidase in Transplantable Murine Lymphoma

Abstract

The reduced glutathione (GSH) levels in the hepatic tissues, extent of lipid peroxidation in the liver, kidney and brain, and alterations in the activity of glutathione peroxidase (GPX) in the hepatic tissues were monitored in mice bearing a transplantable ascitic lymphoma. These markers showed substantial alterations during the height of tumour progression when compared to controls. The GSH level, extent of lipid peroxidation, and GPX activity increased sharply after approximately 2 weeks following inoculation of ascitic cells. This was followed by a steady decline in all markers and death occurred around day 32 after inoculation.

Vanadium: A Modifier of Drug-Metabolizing Enzyme Patterns and Its Critical Role in Cellular Proliferation in Transplantable Murine Lymphoma

“…Similar observations of enhanced GST activity have been reported earlier in human lungs, breast and colon cancers [18][19][20], This increase in GST activity may be related to either tumour invasiveness or alteration in the hepatic environment as the GST enzyme family is neces sary for rapidly proliferating cells [20]. The steady decline in GST activity following the peak may be due to exces sive depletion of reduced glutathione (GSH) [9], since vanadium is known to oxidize NADH by a free-radicalmediated process and to deplete intracellular stores of NADH, NADPH and GSH [21],…”

“…The mice of groups 2 and 7-10 were aseptically inoculated intraperitoneally with DL by transplanting 2 x 106 tumour cells in 0.2 ml saline into each mouse [9].…”

The Catalytic Outcomes of the Constitutive and the Mitogen Inducible Isoforms of Prostaglandin H2 Synthase Are Markedly Affected by Glutathione and Glutathione Peroxidase(s)

“…While selenium-dependent GSH-Pxs have recognized protective roles during pathological conditions resulting in lipid peroxidation, little is known with regard to their ability to regulate cellular prostanoid formation (Buckley et al, 1991;Mirault et al, 1991). It is of interest that, as for COX-2, glutathione peroxidases are modulated during inflammation and tumor development (Pamham et al, 1987;Grisham et al, 1990;Segura-Aguilar et al, 1990;Mirault et al, 1991;Rana et al, 1994). To ascertain the functional significance of the GSH effects described above, samples of COX-1 and COX-2 were incubated with AA and GSH in the presence or absence of a rat liver cytosol preparation, an abundant source of GSH-dependent peroxidases (Burk & Hill, 1993).…”

“…This hypothesis is attractive not only because it provides an additional rationale for the existence of prostaglandin synthase isoforms but, more importantly, it suggests the potential for a selective clinical intervention that precludes changes in the production of those prostanoids necessary for normal body function (Mitchell et al, 1994). It is known that conditions of oxidative stress, such as those associated with inflammatory processes and certain stages of tumor formation, induce the biosynthesis of protective enzymes, including GSH-dependent peroxidase(s) (Pamham et al, 1987;Grisham et al, 1990;Segura-Aguilar et al, 1990;Rana et al, 1994). The differential sensitivities of COX-1 and COX-2 to the action of GSH-dependent glutathione peroxidase(s) suggest that, under these oxidative stress conditions, COX-2 may be responsible for most of the prostanoid biosynthesis in the affected cell and/or organ.…”

Physiological Potential of β-Carotene in Prolonging the Survival of the Host Bearing Transplantable Murine Lymphoma

“…The mice of groups II, VIa, VIla, VIlla, VIb, VIIb, VilIb, IX, and X were aseptically inoculated intraperitonealiy with DL by transplanting 2 x 106 tumor celis/0.2 ml saline into each mouse (13). Group IX and X /3-Carotene (BC), the brick-red colouring principle of carrot, has become one of the focal points of anticancer research in recent times.…”