IL-8→Nitrogen Dioxide→Nitrogen Dioxide→Proinsulin→poly-ADP-ribose

• 19041333(IL-8): SWCNT suppress inflammatory mediator responses in human lung epithelium in vitro.

  This study was carried out in order to evaluate the inflammatory response of immortalised and primary human lung epithelial cells (A549 and NHBE) to single-walled carbon nanotube samples (SWCNT).

• 15003325(Nitrogen Dioxide): Pro-inflammatory responses of human bronchial epithelial cells to acute nitrogen dioxide exposure.

  Nitrogen dioxide (NO2) is an environmental oxidant , known to be associated with lung epithelial injury.

• 11153061(Nitrogen Dioxide): Detection of poly(ADP-ribose) synthetase activity in alveolar macrophages of rats exposed to nitrogen dioxide and ozone.

  The stimulation of polyADPR synthetase activity after O3 exposure or NO2 + O3 exposure reflects a response to lung cellular DNA repair , which may be used as an indicator for assessing DNA damage caused by oxidant injury.

• 6281256(Proinsulin): Protection by superoxide dismutase, catalase, and poly(ADP-ribose) synthetase inhibitors against alloxan- and streptozotocin-induced islet DNA strand breaks and against the inhibition of proinsulin synthesis.

  On the other hand , compounds that inhibit islet nuclear poly (ADP-ribose) synthetase were found to protect against alloxan - as well as streptozotocin-induced inhibition of proinsulin synthesis.

• 6299867(poly-ADP-ribose): Effect of poly(ADP-ribose) synthetase inhibitor administration to rats before and after injection of alloxan and streptozotocin on islet proinsulin synthesis.

  Pretreatment with poly (ADP-ribose) synthetase inhibitors was found to protect against alloxan - or streptozotocin-induced decrease in proinsulin synthesis.