Author(s): Danielle N. Holt

Presentation: oral

Cadmium is a heavy metal released into the environment primarily through the improper disposal of electronic waste. Human exposure to cadmium is linked to the development of bone diseases such as osteoporosis. Our lab researches mechanisms by which cadmium induces apoptosis in bone-forming osteoblasts. One under-investigated area of osteoblast apoptotic signaling is the involvement of lysosomes. We hypothesize that cadmium induces lysosomes to permeabilize, release cathepsins, leading to apoptosis in osteoblast-like cells Saos-2 and MG-63. Cells were treated with 0-10 µM CdCl2 for 24 or 48 hours. Lysosomal permeabilization was visualized using Acridine Orange and lysosomal protease cathepsin b expression was determined using Western blot. CdCl2 treated cells were co-treated or pre-treated with cathepsin b inhibitor CA074Me and viability was assessed using MTT assay. Acridine Orange and MTT results suggest that cadmium does not induce lysosomal permeabilization as a cell death mechanism. Western blot analysis suggests that cadmium induces cathepsin b expression, indicating induced autophagy in osteoblasts. This work furthers understanding of cadmium's effect on lysosomal function and its induced toxicity in bone.

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