NICKEL-INDUCED RENAL LIPID-PEROXIDATION IN DIFFERENT STRAINS OF MICE - CONCURRENCE WITH NICKEL EFFECT ON ANTIOXIDANT DEFENSE SYSTEMS

Lipid peroxidation (LPO) and active oxygen-detoxifying enzymes, atalase (CAT), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD), as well as glutathione (GSH) and some related enzymes, glutathione-S-transferase (GST) and glutathione reductase (GSSG-R) were assayed in kidneys of BALB/cAnNCr (BALB/c), C3H/HeNCr-MTV- (C3H), B6C3F1, and C57BL/6NCr (C57BL) mice 3-48 h after a single intraperitoneal injection of 170-mu-mol nickel (II) acetate (NiAcet)/kg body wt. In control mice that received 340-mu-mol sodium acetate/kg, the levels of enzymes and GSH did not significantly vary in time but were different in various strains. The basal activities of CAT and SOD in the controls were highest in BALB/c and lowest in C57BL mice (1.8:1.0 and 1.4:1.0 respectively) in contrast to that of GSH-Px which was highest in B6C3F1 and lowest in BALB/c (1.3:1.0; P < 0.05). The strain ranking of control concentrations of renal GSH was B6C3F1 > C3H greater-than-or-equal-to C57BL > BALB/c (2.8:2.4:2.3:1.0), and that of GSSG-R was C3H greater-than-or-equal-to C3H greater-than-or-equal-to BALB/c > B6C3F1 greater-than-or-equal-to C57BL (1.5:1.4:1.1:1.0). The basal activity of renal GST in control mice was 25% lower in C3H than in any of the other 3 strains. The renal LPO levels in the control mice did not vary among strains. Nickel treatment transiently increased renal LPO in the BALB/c mice by 100%, in B6C3F1 by 30%, and in C57BL by 20% (P < 0.05), with no significant effect in C3H mice. Thus, the magnitude of nickel-induced renal LPO was greatest in the strain that is lowest in GSH and GSH-Px, but not in CAT and SOD. Nickel effects on GSH and the enzymes were time-dependent and included transient inhibition or enhancement of different proportions with no apparent strain- and/or base level-related patterns, or concurrence with LPO. The results emphasize the importance of GSH and GSH-Px for preventing nickel-induced oxidative cell damage.