The view shared by most researchers is that necrosis is a largely unregulated and not programmed form of cell death in contrast to apoptosis. However, they acknowledge the existence of programmed necrosis (or necroptosis) as a third mode of cellular self-disgesion. If you want to know more there is a recent article here: http://www.ncbi.nlm.nih.gov/pubmed/25455759

Cheers, Christian

Dear Md. Tanjir Islam,

I think this link might help.

https://en.wikipedia.org/wiki/Apoptosis

Dear Colleague,

Apoptosis  is  a  pathway  of  cell  death  in  which  cells  activate enzymes that degrade the cells’ own nuclear DNA and nuclear and  cytoplasmic  proteins. Fragments of the apoptotic cells then break off, giving the appearance that is responsible for the name (apoptosis, “falling off”). Apoptosis differs in this respect from necrosis, which is characterized by loss of membrane integrity, enzymatic  digestion  of  cells,  leakage  of  cellular  contents, and  frequently  a  host  reaction . However,  apoptosis  and  necrosis  sometimes  coexist,  and apoptosis  induced  by  some  pathologic  stimuli  may  progress to necrosis. Apoptosis occurs in many normal situations and serves to eliminate potentially harmful cells and cells that have outlived their usefulness. It also occurs as a pathologic event when  cells  are  damaged  beyond  repair,  especially  when the damage affects the cell’s DNA or proteins; in these situations, the irreparably damaged cell is eliminated.

Thank you Mr. Md. Sahab Uddin and Mr. Jirapat Chunthapong for your response.

Basically necrosis is caused by the external factors but apoptosis from internal factors. Necrosis are abnormal condition but apoptosis could be physiological. Morphologically they are fundamentally different. The necrosis shows karyopyknosis, karyorrhexis, and karyolysis; but the apoptosis features with nuclear condensation, membrane blebing with nuclear fragmentation, and form apoptosis body.

The view shared by most researchers is that necrosis is a largely unregulated and not programmed form of cell death in contrast to apoptosis. However, they acknowledge the existence of programmed necrosis (or necroptosis) as a third mode of cellular self-disgesion. If you want to know more there is a recent article here: http://www.ncbi.nlm.nih.gov/pubmed/25455759

Cheers, Christian

Are you wondering how to test whether your drug is inducing apoptosis or necrosis? 

In addition what say the others:

Caspase activation (in apoptosis) probably represents the most striking difference.

You can have caspase activation when cells are dying by necrosis, but caspase activation is not required for cell death (i.e., inhibitors do not prevent cytotoxicity). 

Rigorous definition of cell death modalities is very complicated. I each case you have to describe biochemical  pathways leading to it together with morphological features. In most cases you can just state I have found a cell death with following biochemical and morphological features....

Nowdays the biochemical criteria are more important than the morphological ones. 

So, the last contribution by Ashley sounds a bit like an oxymoron since  she talk about   "necrosis" based only on morphology  while ignoring biochemical base. 

Here attached is a nice article.

Best regards

Robert

I’m not talking about morphology at all, although there are morphology based assays that suggest apoptosis is occurring (i.e., nuclear blabbing), but these are insufficient alone, especially when wanting to determine the precise mechanism. I’m specifically talking about caspase activation, and whether that is required for cell death. Many people look at caspase activation via immunoblotting and conclude that their agent is inducing apoptosis. I’m arguing that this is not always the case. I have worked on drugs that clearly cause cell lysis. I have a dozen assays showing this. This agent is also causing procaspase 3 --> caspase 3 cleavage, detected via immunoblotting. The question is whether the cytotoxicity is dependent on caspase activation. I.e., if you inhibit caspase activation, does the cell still die? If not, then you’re probably looking at apoptosis (although you will need/want to figure out how, mechanistically, that’s happening). In contrast, if cell death is not altered, then there is something else going on. 

Following with great interest your chats, I think that the three attached article will illustrate at best that each of you is right!

And the biological story is very complex.

Best regards

Robert