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NiCl2-down-regulated antioxidant enzyme mRNA expression causes oxidative damage in the broiler(')s kidney
Hongrui Guo1, Bangyuan Wu, Hengmin Cui
1Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Yaan, China.
Abstract:
The kidney serves as a major organ of nickel (Ni) excretion and is a target organ for acute Ni toxicity due to Ni accumulation. There are no studies on the Ni or Ni compound-regulated antioxidant enzyme mRNA expression in animals and human beings at present. This study was conducted to investigate the pathway of nickel chloride (NiCl2)-caused renal oxidative damage by the methods of biochemistry, quantitative real-time polymerase chain reaction, and enzyme-linked immunosorbent assay. Two hundred and eighty one-day-old broilers were randomly divided into four groups and fed on a control diet and three experimental diets supplemented with 300, 600, and 900 mg/kg of NiCl2 for 42 days. Dietary NiCl2 elevated the malondialdehyde (MDA), nitric oxide (NO), 8-hydroxy-2'-deoxyguanosine (8-OHdG) contents, and reduced the ability to inhibit hydroxy radical in the NiCl2-treated groups. Also, the renal inducible nitric oxide synthase (iNOS) activity and mRNA expression levels were increased. The total antioxidant (T-AOC) and activities of antioxidant enzymes including copper zinc superoxide dismutase (CuZn-SOD), manganese superoxide dismutase (Mn-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), glutathione reductase (GR), and glutathione-s-transferase (GST) were decreased, and the glutathione (GSH) contents as well were decreased in the kidney. Concurrently, the renal CuZn-SOD, Mn-SOD, CAT, GSH-Px, GST, and GR mRNA expression levels were decreased. The above-mentioned results showed that dietary NiCl2 in excess of 300 mg/kg caused renal oxidative damage by reducing mRNA expression levels and activities of antioxidant enzymes, and then enhancing free radicals generation, lipid peroxidation, and DNA oxidation.
Insights
Dietary nickel chloride (NiCl2) causes kidney oxidative damage in broilers by reducing antioxidant enzyme mRNA expression and activity. This leads to increased free radicals, lipid peroxidation, and DNA oxidation at levels exceeding 300 mg/kg.
Area of Science:
- Environmental Toxicology
- Renal Physiology
- Oxidative Stress Mechanisms
Background:
- The kidney is a primary site for nickel (Ni) excretion and is susceptible to Ni toxicity.
- No prior studies have investigated Ni or Ni compound-regulated antioxidant enzyme mRNA expression in animals or humans.
Purpose of the Study:
- To investigate the pathway of nickel chloride (NiCl2)-induced renal oxidative damage.
- To analyze the effects of NiCl2 on antioxidant enzyme mRNA expression and activity in broilers.
Main Methods:
- Biochemistry, quantitative real-time PCR, and ELISA were employed.
- Broilers were fed diets with varying NiCl2 concentrations (0, 300, 600, 900 mg/kg) for 42 days.
- Assessed oxidative stress markers, nitric oxide synthase activity, and antioxidant enzyme levels and gene expression.
Main Results:
- NiCl2 elevated malondialdehyde (MDA), nitric oxide (NO), and 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, while reducing hydroxy radical inhibition.
- Renal inducible nitric oxide synthase (iNOS) activity and mRNA expression increased.
- Activities and mRNA expression of antioxidant enzymes (CuZn-SOD, Mn-SOD, CAT, GSH-Px, GR, GST) and glutathione (GSH) content decreased.
Conclusions:
- Dietary NiCl2 above 300 mg/kg induces renal oxidative damage in broilers.
- This damage results from reduced antioxidant enzyme expression and activity, leading to enhanced free radical generation, lipid peroxidation, and DNA oxidation.
