Protective Effect Of Copper Research Articles

Protective Effect of Copper (I)-Nicotinate Complex on DAB-Induced Hepatocellular Carcinoma in Rats

The aim of the present work was to evaluate the effect of copper (I)-nicotinate complex (CNC) on experimentally 4-Dimethylaminoazobenzene (DAB)-induced hepatocellular carcinoma (HCC) in male rats. In addition to the histopathological examination we measured hepatic glutathione content, malondialdehyde, nitric oxide levels, lamin B1 m-RNA, caspase-3 activity and serum interleukin-12 level after 2, 4, 6, 8 months from commencement of the experiment. Results: histopathological examination showed HCC development after 4 months of DAB administration. The hepatic glutathione content, lamin B1 m-RNA and nitric oxide levels were significantly elevated, while malondialdehyde, interlukin-12 levels and caspase-3 activity were significantly decreased with the progression and development of the HCC. On the other hand, administration of CNC one month before DAB delayed the development of neoplastic growth to the 8th month. Interestingly, when CNC was administered one month after DAB, it successfully prevented HCC development throughout the whole experiment as confirmed by histopathological data and explained by biochemical markers, as glutathione, lamin B-1 and nitric oxide were significantly declined but malondialdehyde, interlukin-12 and caspase-3 activity were significantly elevated compared to that in corresponding control group. Conclusion: CNC was able to delay or prevent HCC development in rats fed with the potent liver carcinogen DAB. Our data shows that CNC exerts its anti-tumour effects through modulating oxidative stress status as well as the machinery of apoptosis and angiogenesis. Therefore, CNC may be used as a potential protective anticancer agent.

Chromium-induced hearing loss in rats and the protective effect of copper and manganese

Chromium-induced hearing loss in rats and the protective effect of copper and manganese

Lead-Induced Hearing Loss in Rats and the Protective Effect of Copper

Lead is a common environmental pollutant which can induce various toxic effects to humans and/or animals. This work aimed to study the hearing loss in rats induced by lead and the protective effect of copper. The auditory brainstem response (ABR) was used to study the hearing loss in rats. The results showed that lead prolonged the latencies of wave I to V of ABRs of the rats but did not affect the interpeak latencies of waves I-III, III-V, and I-V, indicating that lead could cause hearing loss in rats by impairing the cochlea. After receiving copper, the quality and the wave latencies of the ABR of the rats were restored to a certain extent, indicating that copper played a protective role in lead-induced hearing impairment. The mechanisms were also proposed that lead could cause hearing loss in rats mainly through damaging the cochlea component, and copper might antagonize the toxicity of lead in three primary ways.

Protective effect of copper against cadmium cytotoxicity on cultured vascular endothelial cells

We investigated the effect of copper on cadmium-induced cytotoxicity on vascular endothelial cells from bovine aorta in a culture system. Cytotoxicity was evaluated by the [ 3H]adenine release assay and the histological observation. After a 24-h incubation, cadmium exhibited a significant cytotoxicity on confluent cultures of endothelial cells in a dose-dependent manner, while copper only slightly did after a 24-h incubation. It was found that copper (5 μM) significantly decreased cadmium (1 and 2 μM) cytotoxicity; histologically, formation of de-endothelialized areas in the cell layer caused by cadmium was reduced by copper. The accumulation of cadmium in the cell layer was significantly decreased by copper; however, that of copper was unaffected by cadmium. It was therefore suggested that copper significantly protects cadmium-induced cytotoxicity on cultured endothelial cells primarily through decreasing the cellular cadmium accumulation.

Protective effect of copper against pancreatic insult in streptozotocin-induced diabetogenic rat

The present study examined the alterations in endogenous oxy-radical scavenging system of pancreatic tissue associated with the dose of 45 mg/kg streptozotocin (STZ) alone or with various combinations. The activities of pancreatic Mn-superoxide dismutase (SOD) and catalase were no apparent changes in the other groups except for the Cu(II) 4 mg/kg pretreated group. The presence of 4 mg/kg of Cu(II) with or without 125 mg/kg of diethylenetriaminepentaacetic acid (DTPA) markedly attenuated the fall in activity of Cu, Zn-SOD by STZ stress. In particular, STZ-induced superoxide generation was dramatically abolished by prior administration of Cu(II) 4 mg/kg. Conclusively, We suggest the possible involvement that copper may enhance the defense mechanism of pancreatic oxidative damage by STZ challenge.

Protective effect of copper (II) against lipid peroxidation and hemolysis of pig and hamster erythrocytes of different vitamin E status induced by tween 20, ascorbate, and/or azide

Protective effect of copper (II) against lipid peroxidation and hemolysis of pig and hamster erythrocytes of different vitamin E status induced by tween 20, ascorbate, and/or azide

Copper protects against galactosamine-induced hepatitis

Although copper is believed to be hepatotoxic in Wilson's disease and Indian Childhood Cirrhosis (ICC), the rat shows only minimal hepatic damage on copper-loading. To investigate the possibility that copper deposition may potentiate the effects of a superimposed hepatitis, D-galactosamine (GalN) was given to copper-loaded and control rats. In the non-copper-dosed rats, GalN 0.85 g/kg i.p. produced elevated serum AST (3731 +/- 545 IU/l; normal 64.8 +/- 2.1), ALT (2090 +/- 190 IU/l; normal 18.0 +/- 0.7), and OCT (16.7 +/- 2.6 mmol/min/ml; normal 0.12 +/- 0), and liver cell necrosis with portal infiltration. In rats whose liver copper was elevated to 1298 +/- 169 micrograms/g (control 18.7 +/- 1.7) by oral copper supplementation, GalN produced much smaller increases in AST (825 +/- 122 IU/l), ALT (103 +/- 15 IU/l) and OCT (0.27 +/- 0.02 mmol/min/ml) and minimal histological damage. Viable bacterial cell counts from faecal homogenates showed that the anaerobically cultured bacteria were reduced on copper-dosing of rats. Therefore the protective effect of copper may be due to a decrease in gut-derived endotoxin acting on the liver, or to an impaired prostaglandin synthesis or perhaps to synthesis of acute phase reactants.

Protective role of trace metals in lead intoxication

Protective effect of copper (Cu), zinc (Zn) or cobalt (Co) against lead (Pb) toxicity in rats was investigated. Trace metal administration together with Pb decreased the hepatic and renal uptake of lead and reduced the Pb-induced inhibition of blood δ-aminolevulinic acid dehydratase (δ-ALAD) activity. The hepatic uptake of Zn or Co was also increased in animals administered Pb and Zn or Pb and Co, respectively. However, no significant difference could be observed between the protective effects of three essential trace metals examined against lead toxicity.