In Vivo Studies of Molybdenum-Induced Apoptosis in Kidney Cells of Caprine

Abstract

Molybdenum (Mo) is an essential microelement for the health of animals and human beings, and high dietary intake of Mo can lead to pathological conditions. However, the cytotoxic effects of high levels of Mo on the renal cells in ruminants have not been reported. Therefore, this in vivo study in goats was designed to investigate the impact of Mo on kidney-related apoptosis genes, and histopathological and ultrastructural changes in renal cells using real-time quantitative polymerase chain reaction (RT-qPCR), light microscopy, and transmission electron microscopy. A total of 48 goats were randomly distributed in equal number into four groups and assigned with one of three oral treatments of ammonium molybdate (15, 30, and 45 mg Mo kg(-1) BW), while control group received no Mo. Kidney tissues were taken from individual goat at days 0, 25, and 50 for determining expression of apoptosis genes including Bax, Bcl-2, Cyt c, caspase-3, and Smac. The results revealed that the expression of Bax, Smac, Cyt c, and caspase-3 was significantly (P < 0.05 or P < 0.01) upregulated in renal cells, whereas Bcl-2 was downregulated (P < 0.01). Histopathological lesions showed degeneration of renal tubule, glomerular atrophy, and dilation of Bowman's capsule. In addition, ultrastructural injury that predicted varying degrees of vacuolization, irregularity, fission of the nucleus, and swelling of mitochondria was observed in the cytoplasma of cells in groups treated with 30 and 45 mg Mo kg(-1). This concluded that high levels of molybdenum, which induces apoptosis of caprine renal cells, might be involved in the mitochondrial intrinsic pathway.

Alterations in antioxidant function and cell apoptosis in duck spleen exposed to molybdenum and/or cadmium

“…It was previously reported that Cd could trigger liver cell apoptosis through activation of Caspase-3A [10], and Cd can induce apoptosis of chicken splenic lymphocytes by increasing mRNA levels of Bak, Caspase-3, and Caspase-9 and by decreasing Bcl-2 [19]. Additionally, high levels of Mo can result in unregulated expression of Bax, CytC, and Caspase-3, whereas it downregulates Bcl-2 in goat kidney [12]. Mo administration has induced an increase in Bax expression and a decrease in Bcl-2 expression in chicken kidney cells [39].…”

“…Mo nanoparticles have induced intracellular reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP) changes, cell cycle arrest, and DNA damage [30]. Additionally, high levels of Mo can cause renal tubule degeneration, glomerular atrophy, nuclei deformation, and fracture in goat kidney [12]. …”

The Co-induced Effects of Molybdenum and Cadmium on Antioxidants and Heat Shock Proteins in Duck Kidneys

“…A deficiency or excess of Mo can cause damage to the body. Several minerals like arsenic, cadmium, lead and mercury are well known to be harmful to the well-being of animals and humans while many other metals, like chromium, manganese, molybdenum or selenium, are necessary but could be harmful over certain levels [2]. Molybdenum ores and fuel containing Mo are widely used in human activities (such as coal combustion), increasing the circulation of Mo in the environment.…”

Interaksi Molekuler Amonium Hidroksida

“…Entropi molar standar mempunyai satuan Joule per mol kelvin (J/molK). Nilai S 0 bersifat absolut, tidak seperti entalpi pembentukan (160)(161)(162)(163)(164)(165) . Dimana keadaan standar suatu unsur nilainya tidak sama dengan nol yang pasti S berada pada suhu ruanagn.Struktur kristal murni mempunyai nilai entropi 0 J/molK pada suhu 0 K, menurut hukum termodinamika ketiga (166)(167)(168)(169) .…”