Maize (Zea mays) seedlings were exposed for 6 h to strong irradiance (1 000 μmol m-1 s-1 of PPFD) at 5, 12, 17, or 25 °C, followed by an exposure to the darkness for 6 h at 22 °C. Leaf chlorophyll fluorescence, net photosynthetic rate (PN), and the amount of superoxide radicals (O2-⋅) in relation to chilling-induced photoinhibition were investigated. During the photophase, a good correlation (r=-0.879) was observed between ΦPS2 (relative quantum efficiency of PS2 electron transport) and the amount of O2-⋅. Treatment with exogenous O2-⋅ reduced the PN and ΦPS2 as the chilling stress did, that was inhibited by specific scavenger of O2-⋅. Hence chilling-induced photoinhibition might be due to the production of O2-⋅. In contrast, in the dark period, PN and ΦPS2 of the seedlings treated with the exogenous O2-⋅ were enhanced, but they were inhibited by the specific scavenger of O2-⋅, showing the photoprotective role of O2-⋅ in the recovery phase. Furthermore, in terms of the effect of exogenous O2-⋅ on the xanthophyll cycle, the O2-⋅ production suggested a promotion effect for the de-epoxidation of violaxanthin during the photophase, the epoxidation of zeaxanthin at the dark stage, and the increase of the xanthophyll pool both in the photophase and dark phase, resulting in an enhancement of the ability of non-photochemical quenching to avoid or alleviate the damage to photosynthetic apparatus. and D. Ke, G. Sun, Y. Jiang.
One of the significant limiting complications of paclitaxel is
painful peripheral neuropathy during its therapy for several types
of cancers. Our recent study showed that impairment of
Nrf2-antioxidant response element (Nrf2-ARE) and upregulation
of oxidative signals in the dorsal root ganglion (DRG) of rats with
treatment of paclitaxel result in neuropathic pain. The purpose of
this study was to examine the beneficial role played by
electroacupuncture (EA) in modifying neuropathic pain evoked by
paclitaxel via Nrf2-ARE and oxidative mechanisms. Behavioral
test was performed to determine mechanical and thermal
sensitivity in rats. Western Blot analysis and ELISA were used to
examine expression of Nrf2-ARE and superoxide dismutases
(SOD); and the levels of products of oxidative stress in the DRG.
Our data showed that paclitaxel increased mechanical and
thermal sensitivity and this was accompanied with impaired
Nrf2-ARE and SOD in the DRG and amplified products of
oxidative stress (i.e. 8-isoprostaglandin F2α and 8-hydroxy-2’-
deoxyguanosine). EA treatment largely restored the levels of
Nrf2-ARE/SOD and inhibited products of oxidative stress and
thereby attenuated mechanical and thermal hypersensitivity
induced by paclitaxel. In conclusion, we revealed specific
signaling pathways leading to paclitaxel-evoked neuropathic pain,
including impairment of Nrf2-ARE and heightened oxidative
signals. We further provided evidence for the role of EA in
alleviating paclitaxel-neuropathic pain via these molecular
mediators.
Paclitaxel is used for the treatment of several types of cancers.
However, one of the significant limiting complications of
paclitaxel is painful peripheral neuropathy during its therapy. In
this study we examined the engagement of antioxidative signal
pathway of the dorsal root ganglion (DRG) in mechanical and
thermal hypersensitivity evoked by paclitaxel. Behavioral test was
performed to determine mechanical and thermal sensitivity in
rats. Western blot analysis and ELISA were used to examine
expression of Nrf2-antioxidant response element (ARE) and
superoxide dismutases (SOD); and the levels of products of
oxidative stress in the DRG. Our results show that paclitaxel
increased mechanical and thermal sensitivity as compared with
vehicle control animals. Paclitaxel also impaired Nrf2-ARE and
SOD in the DRG and amplified products of oxidative stress,
namely 8-isoprostaglandin F2α and 8-hydroxy-2’-
deoxyguanosine. Systemic administration of SOD mimetic using
tempol, antioxidant vitamin C or blocking oxidative pathway
using NADPH oxidase inhibitor (GKT137831) attenuated
mechanical and thermal hypersensitivity induced by paclitaxel.
This inhibitory effect was accompanied with decreases of
proinflammatory cytokines (PICs) such as IL-1β, IL-6 and TNF-α
in the DRG. In conclusion, the data revealed impairment of
Nrf2-ARE and heightened oxidative and PIC signals in the DRG of
paclitaxel rats, leading to neuropathic pain. Balancing of reactive
oxygen species by supplying antioxidants and/or inhibiting
NADPH oxidase appears significant to yield beneficial effects in
neuropathic pain conditions after chemotherapeutic paclitaxel.