Pluchea lanceolata attenuates cadmium chloride induced oxidative stress and genotoxicity in Swiss albino mice

Abstract

Cadmium intoxication induces lipid peroxidation and causes oxidative damage to various tissues by altering antioxidant defence system enzymes. At 24 h after treatment with a single intraperitoneal dose of cadmium chloride (5 mg kg-1), Swiss albino mice showed a significant increase in the levels of malanodialdehyde and xanthine oxidase (P<0.001), and a concomitant depletion of renal glutathione, catalase (P<0.001) and other antioxidant enzymes. CdCl2 also led to a simultaneous increase in micronuclei formation (P<0.001) and chromosomal aberrations (P<0.05) in mouse bone marrow cells. Oral pre-treatment with Pluchea lanceolata extract at doses of 100 and 200 mg kg-1 for 7 consecutive days before CdCl2 intoxication caused a significant reduction in malanodialdehyde formation and xanthine oxidase activity (P<0.001). A significant restoration of the activity of antioxidant defence system enzymes such as catalase, glutathione peroxidase (P<0.05), glutathione-S-transferase and glutathione reductase (P<0.001) was observed. A significant dose-dependent decrease in chromosomal aberrations and micronuclei formation was also observed (P<0.05). The results indicate that pre-treatment with P. lanceolata attenuates cadmium chloride induced oxidative stress and genotoxicity by altering antioxidant enzymes and reducing chromatid breaks and micronuclei formation.

Quercetin Protects against Cadmium-Induced Renal Uric Acid Transport System Alteration and Lipid Metabolism Disorder in Rats

“…The kidney is a target organ for Cd; therefore, it was necessary to investigate the effects of Cd on renal XOR activity and UA transport-related proteins in rats. Being consistent with activated renal XO in Cd-exposed Swiss albino mice [33, 34], the present study confirmed activation of renal XO in Cd-exposed Sprague-Dawley rats with a significant reduction of renal XDH/XO ratio, which resulted from the increased XO activity with the relatively decreased XDH activity. These data further demonstrates that Cd enhances the conversion of XDH to XO [7] in the kidney of rats, possibly causing serious renal damage induced by XOR hyperactivity-mediated ROS.…”

Benzo(a)pyrene-induced genotoxicity: Attenuation by farnesol in a mouse model

“…Early reports strongly support that soya isoflavones protect against B(a)P induced toxicity [4]. In our recent findings we have shown the role of pluchea lanceolata in attenuating genotoxicity of cadmium chloride [18].…”

Investigation of lipid peroxidation as probable mechanism of rifampicin toxicity in vivo

“…6 The study of Ebuehi et al 12 had also shown that presence of free radicals may be one of the plausible explanations for elevated MDA levels; also catalytic actions of anti-oxidants enzymes are important for the effective removal of oxygen radicals. The aforementioned facts are consistent with the report of Jahangir et al 13 that showed that enhanced catalase activity may be a protective mechanism against cadmium toxicity. The results obtained from the present study although it showed a low, non-significant (p > 0.05) increase in the Malondialdehyde (MDA) level of the testes (63.10±4.99); serum (65.86±4.33); liver (45.13±1.62) and brain (46.03±1.60) of Rif treated group compared with the control (60.97±3.51; 59.92±5.29; 44.01±2.67; 45.11±2.62) respectively, it is an indication that Rif induced free radical generation.…”

“…This suggests a reduced level of endogenous antioxidants and subsequent toxicity on cells. These findings may strengthen the studies of Ebuehi et al 12 and Jahangir et al 13 to propose that Rif toxicity may be via free radical generation. However, the low, non-significant (p > 0.05) increase in the Malondialdehyde (MDA) levels in the testes, serum, brain and liver indicates that Rif toxicity may also be through other toxication mechanisms such as direct toxicity of cells, cellular dysfunction, conversion of Rif to electrophiles, nucleophiles and redox-active reactants, 1 other than only via lipid peroxidation.…”