The Association between Splenocyte Apoptosis and Alterations of Bax, Bcl-2 and Caspase-3 mRNA Expression, and Oxidative Stress Induced by Dietary Nickel Chloride in Broilers

Abstract

Two hundred and forty avian broilers were equally divided into four groups, and raised with a corn-soybean basal diet or the same diet supplemented with 300, 600, 900 mg/kg NiCl2 for 42 days. Numbers or percentages of apoptotic splenocytes by flow cytometry (FCM) and TUNEL were higher (p < 0.05 or p < 0.01) in the 300, 600 and 900 mg/kg groups than those in the control group. Results measured by qRT-PCR and ELISA showed that mRNA expression and contents were significantly higher (p < 0.05 or p < 0.01) in Bax and Caspase-3, and were significantly lower (p < 0.05 or p < 0.01) in Bcl-2 of the 300, 600 and 900 mg/kg groups. Also, the SOD, CAT and GSH-Px activities, and the ability to inhibit hydroxyl radical, and GSH contents were significantly decreased (p < 0.05 or p < 0.01), and MDA contents were increased (p < 0.05 or p < 0.01) in all groups. In conclusion, dietary NiCl2 in excess of 300 mg/kg caused apoptosis, altered Bax, Bcl-2 and Caspase-3 mRNA expression levels and contents, and induced oxidative stress in the spleen. Also, splenocyte apoptosis was closely related to the alternations of Bax, Bcl-2 and Caspase-3 mRNA expression, and oxidative damage. The splenic immunity and blood filtration functions were impaired in broilers.

Antioxidant Systems in Poultry Biology: Superoxide Dismutase

“…In contrast to the aforementioned results, Cd oral administration produced peroxidative damage in chickens, as indicated by increase in TBARS, reduction in GSH concentration in liver and kidney, but increased CAT and SOD activities were observed in erythrocytes [144]. Dietary nickel chloride is also shown to have a negative effect on SOD and other antioxidant enzymes (GSH-Px and CAT) in the intestine [145], cecal tonsil [146] or splenocytes [147]. Similarly, vanadium inhibited SOD activity in chicken liver and kidney [148].…”

Nickel Chloride (NiCl2) Induces Histopathological Lesions via Oxidative Damage in the Broiler’s Bursa of Fabricius

“…Chen et al [17] have reported that NiCl 2 could induce oxidative toxicity in human lymphocytes. Our previous studies have also shown that dietary NiCl 2 in excess of 300 mg/kg causes splenic, intestinal, cecal tonsil, renal, and thymic oxidative damage and/or lesions [18][19][20][21][22]. It is also showed that NiCl 2 in excess of 300 mg/kg causes serum oxidative stress in broilers in our previous study [23].…”

Effects of Nickel Chloride on Histopathological Lesions and Oxidative Damage in the Thymus

“…As the first line of cellular defence against oxidative damage, SOD and CAT play an important role in these enzymatic mechanisms [26]. SOD can break up ROS and repair cellular damage caused by ROS [16]. CAT is responsible for the breakdown of hydrogen peroxide (H 2 O 2 ) [27].…”

“…Living organisms possess several antioxidative agents (including enzymes such as SOD, GSH-Px, and CAT, Data are presented with the mean ± standard deviation (n = 5). GSH, and the ability to inhibit hydroxyl radical, and nonenzymatic antioxidants such as extra calcium and vitamin E) and protect them against the harmful effect of oxidative stress [16] [21] [22]. These antioxidants inhibit overproduced free radicals (including ROS and .…”

“…NiCl 2 -induced human lymphocyte toxicity may be mediated by oxygen radical intermediates [15]. Our previous studies have also shown that dietary NiCl 2 causes intestinal and splenic oxidative damage [12] [16]. However, very limited data are available on the oxidative damage induced by dietary NiCl 2 in the thymus in human beings and animals.…”