Effects of Antioxidants on Induction of Apoptosis in Bursal Cells of Fabricius during In Vitro Cultivation

Abstract

ABSTRACT. After physically disrupting cell contacts, apoptosis of bursal cells of Fabricius was induced during in vitro cultivation. The percentage of apoptotic cells increased with incubation time and approximately 70% cells represented apoptosis after 6 hr of incubation. The induction of apoptosis was significantly inhibited by treatment of the cells with ascorbic acid (vitamin C), but not with trolox, a vitamin E analog. An intense DNA ladder pattern was shown at 6 hr post-isolation, which is a biochemical hallmark of apoptosis. Treatment of the cells with ascorbic acid inhibited the DNA fragmentation, but trolox did not. To monitor the intracellular production of reactive oxygen species (ROSs), the intensity of fluorescence emitted from DCFH-DA was measured. The intensity of fluorescence from cells incubated for 0.5-2 hr was approximately 2-fold higher than that from cells at 0 hr. The relative intensity of fluorescence decreased immediately after the addition of ascorbic acid to the cells. The intensity from the cells treated with ascorbic acid was 20-30% of that from the control cells at each incubation time. For trolox, the intensity was 50-70% of that from the control cells at each 1 to 2 hr incubation time. When ROSs-induced lipid peroxidation was assessed using cis-parinaric acid (PnA) as a monitor molecule, lipid peroxidation was found to occur in the control cells after isolation of the bursal cells. Treatment of the cells with trolox reduced lipid peroxidation, but treatment with ascorbic acid enhanced peroxidation.-KEY WORDS: antioxidant, apoptosis, bursa of Fabricius, in vitro culture, reactive oxygen species.

Bursa atrophy at 28 days old caused by variant infectious bursal disease virus has a negative economic impact on broiler farms in Japan

“…PG broilers may be more susceptible to IBDV because BB ratios of PG broilers were slightly lower than those of NG broilers. Apoptosis occurs in BF due to pathological and physiological stimuli, chemical and physical agents (Arai et al, 2000). Some apoptosis, cystic lesions and infolding epithelium into lymphoid follicles were also seen at 14 d in PG broilers of the second flock before IBDV introduction.…”

Satratoxin H Generates Reactive Oxygen Species and Lipid Peroxides in PC12 Cells

“…The accumulation of ROS generation causes lipid peroxidation as previously described. 37,43) Similarly, ROS production followed by the production of lipid peroxides such as 4-hydroxynonenal, and MDA has been found in PC12 cells after the exposure to 200 mM H 2 O 2 for 24 h or to toxic chemical dieldrin. 44,45) GSH neutralizes H 2 O 2 in the cytosol and the mitochondria, 15,29,46) and detoxifies lipid peroxidation products.…”

Structural and Functional Consequences of Trolox C Treatment in the Rat Model of Postnatal Hyperoxia

“…34 Recent in vitro studies carried out on cultured bursal cells and neurons in which cell death occurred resulting from oxidative stress suggest that trolox C could have a protective effect against necrosis but none against apoptosis. [35][36][37] Other studies, however, have concluded that trolox C was successful, for example, in reducing apoptosis in mouse thymocytes, rabbit myocytes, and anterior pituitary cells. 38 -40 It will be useful to investigate the presence of apoptotic and necrotic markers in OIR to better understand the predominant mode of neuronal cell death taking place in this model and, more specifically, the implications on rod and cone pathways.…”