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Liver Cells

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Liver Cells

Postby swallow08 » Sat May 14, 2005 11:04 pm

do liver cells have mitochondria?
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Postby Poison » Sun May 15, 2005 2:24 pm

What's different for liver cells? :shock: All eukaryotic cells have mitochondria. So, yes. They have.
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Postby MrMistery » Sun May 15, 2005 5:56 pm

A hepatocyte has about 1000 mitochondria.
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Postby Dr.Stein » Tue Jul 12, 2005 9:40 am

Yes, hepatocytes is one of several "hard-worked" cells. Considering to their functions, they need extra energy to work, so they are equipped with a lot of mitochondria, in which they generate 38 ATP, more 2 ATP compared to "regular" cells.
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Postby victor » Tue Jul 12, 2005 1:02 pm

Extra 2 ATPs for the work as bonuses..
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Postby chemistry_freako » Tue Jul 12, 2005 3:14 pm

Yea, for all the work they do, mitochondria (aka the powerhouse) are definitely present to provide the hepatocytes with ATP =D
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Postby MrMistery » Sat Jul 16, 2005 7:16 pm

Dr.Stein wrote:Yes, hepatocytes is one of several "hard-worked" cells. Considering to their functions, they need extra energy to work, so they are equipped with a lot of mitochondria, in which they generate 38 ATP, more 2 ATP compared to "regular" cells.

What do you mean by that? What differes in the mechanism?
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Postby Dr.Stein » Sun Jul 17, 2005 2:50 am

The mechanisms is similar: glycolysis - TCA cycle - ETS, but there is a little different in converting NADH and FADH2 in the last reactions, so the final product will be different, with extra 2 ATPs.
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Postby MrMistery » Sun Jul 17, 2005 8:54 pm

Oh yeah... The malat dehidrogenase thingy... Forgot about that...
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ok lets see

Postby ginny » Mon Jul 18, 2005 11:53 pm

do liver cells have mitochondria?

It is found that mitochondia lost its transmembrane potential before nuclear apoptotic changes occur. This specific pre-apoptotic collapse of membrane potential is detected in many cell types. It is mediated through permeability transition (PT) pores, a complicated proteinous megachannel that allows for the dissipation of inner membrane ion gradients. Significant data suggest that the PT is central to apoptotic processes[22]. PT will cause the release of caspases activators, cytochrome c or apoptosis inducing factor (AIF). Recent studies have demonstrated that Bcl-2 inhibits apoptosis by preventing release of cytochrome c from mitochondria[23],[24]. Bax, a proapoptotic member of Bcl-2 family, triggers apoptosis by binding to PT pore causing the increase of mitochondrial membrane permeability and release of cytochrome c[25]. Whether there are any other factors existing in mitochondria that can introduce apoptosis in addition to cytochrome c is an open question. Just recently, Susin et al reported that the AIF was purified and sequenced[26],[27].

In current studies, mitochondria were isolated and purified from mouse liver and spinach leaves. When added into egg extracts of Xenopus laevis, they caused nuclei of mouse liver to undergo apoptotic changes. Chromatin condensation, margination and DNA ladder were observed. By incubating isolated mitochondria in some hypotonic solutions, and centrifuging these mixtures at high speed, we got mitochondrial supernatants. We found that in the absence of cytosolic factor, the supernatant alone was able to elicit the apoptotic changes in nuclei. The effective components were partly of protein. DNA fragmentation was partly inhibited by caspase inhibitors AC-DEVD-CHO and AC-YVAD-CHO. Meanwhile, caspase inhibitors fully blocked chromatin condensation. Primary characterization of the nuclear endonuclease(s) induced by mitochondrial supernatants was also conducted. It was found that this endonuclease is different from endonuclease G, cytochrome c-induced nuclease, or Ca2+-activated endonuclease.

Hope that helped in some way let me know If I helped byeee.
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