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2.
We report the existence of a tip-high reactive oxygen species (ROS) gradient in growing Fucus serratus zygotes, using both 5-(and 6-) chloromethyl-2′,7′-dichlorodihydrofluorescein and nitroblue tetrazolium staining to report
ROS generation. Suppression of the ROS gradient inhibits polarized zygotic growth; conversely, exogenous ROS generation can
redirect zygotic polarization following inhibition of endogenous ROS. Confocal imaging of fluo-4 dextran distributions suggests
that the ROS gradient is interdependent on the tip-high [Ca 2+] cyt gradient which is known to be associated with polarized growth. Our data support a model in which localized production of
ROS at the rhizoid tip stimulates formation of a localized tip-high [Ca 2+] cyt gradient. Such modulation of intracellular [Ca 2+] cyt signals by ROS is a common motif in many plant and algal systems and this study extends this mechanism to embryogenesis. 相似文献
4.
In this study we used tightly-coupled mitochondria from Yarrowia lipolytica and Dipodascus ( Endomyces) magnusii yeasts. The two yeast strains are good alternatives to Saccharomyces cerevisiae, being aerobes containing well-structured mitochondria (thus ensuring less structural limitation to observe their appreciable
swelling) and fully competent respiratory chain with three invariantly functioning energy conservation points, including Complex
I, that can be involved in induction of the canonical Ca 2+/P i-dependent mitochondrial permeability transition (mPTP pore) with an increased open probability when electron flux increases
(Fontaine et al. J Biol Chem 273:25734–25740, 1998; Bernardi et al. FEBS J 273:2077–2099, 2006). High-amplitude swelling and collapse of the membrane potential were used as parameters for demonstrating pore opening.
Previously (Kovaleva et al. J Bioenerg Biomembr 41:239–249, 2009; Kovaleva et al. Biochemistry (Moscow) 75:297–303, 2010) we have shown that mitochondria from Y. lipolytica and D. magnusii were very resistant to the Ca 2+ overload combined with varying concentrations of P i, palmitic acid, SH-reagents, carboxyatractyloside (an inhibitor of ADP/ATP translocator), as well as depletion of intramitochondrial
adenine nucleotide pools, deenergization of mitochondria, and shifting to acidic pH values in the presence of high [P i]. Here we subjected yeast mitochondria to other conditions known to induce an mPTP in animal and plant mitochondria, namely
to Ca 2+ overload under hypoxic conditions (anaerobiosis). We were unable to observe Ca 2+-induced high permeability of the inner membrane of D. magnusii and Y. lipolytica yeast mitochondria under anaerobic conditions, thus suggesting that an mPTP-like pore, if it ever occurs in yeast mitochondria,
is not coupled with the Ca 2+ uptake. The results provide the first demonstration of ATP-dependent energization of yeast mitochondria under conditions
of anaerobiosis. 相似文献
5.
In this study we used tightly-coupled mitochondria from Yarrowia lipolytica and Dipodascus ( Endomyces) magnusii yeasts, possessing a respiratory chain with the usual three points of energy conservation. High-amplitude swelling and collapse
of the membrane potential were used as parameters for demonstrating induction of the mitochondrial permeability transition
due to opening of a pore (mPTP). Mitochondria from Y. lipolytica, lacking a natural mitochondrial Ca 2+ uptake pathway, and from D. magnusii, harboring a high-capacitive, regulated mitochondrial Ca 2+ transport system (Bazhenova et al. J Biol Chem 273:4372–4377, 1998a; Bazhenova et al. Biochim Biophys Acta 1371:96–100, 1998b; Deryabina and Zvyagilskaya Biochemistry (Moscow) 65:1352–1356, 2000; Deryabina et al. J Biol Chem 276:47801–47806, 2001) were very resistant to Ca 2+ overload. However, exposure of yeast mitochondria to 50–100 μM Ca 2+ in the presence of the Ca 2+ ionophore ETH129 induced collapse of the membrane potential, possibly due to activation of the fatty acid-dependent Ca 2+/nH +-antiporter, with no classical mPTP induction. The absence of response in yeast mitochondria was not simply due to structural
limitations, since large-amplitude swelling occurred in the presence of alamethicin, a hydrophobic, helical peptide, forming
voltage-sensitive ion channels in lipid membranes. Ca 2+- ETH129-induced activation of the Ca 2+/H +-antiport system was inhibited and prevented by bovine serum albumin, and partially by inorganic phosphate and ATP. We subjected
yeast mitochondria to other conditions known to induce the permeability transition in animal mitochondria, i.e., Ca 2+ overload (in the presence of ETH129) combined with palmitic acid (Mironova et al. J Bioenerg Biomembr 33:319–331, 2001; Sultan and Sokolove Arch Biochem Biophys 386:37–51, 2001), SH-reagents, carboxyatractyloside (an inhibitor of the ADP/ATP translocator), depletion of intramitochondrial adenine nucleotide
pools, deenergization of mitochondria, and shifting to acidic pH values in the presence of high phosphate concentrations.
None of the above-mentioned substances or conditions induced a mPTP-like pore. It is thus evident that the permeability transition
in yeast mitochondria is not coupled with Ca 2+ uptake and is differently regulated compared to the mPTP of animal mitochondria. 相似文献
6.
Ischemic postconditioning (PostC) is known to reduce cerebral ischemia/reperfusion (I/R) injury; however, whether the opening of mitochondrial ATP-dependent potassium (mito-KATP) channels and mitochondrial permeability transition pore (mPTP) cause the depolarization of the mitochondrial membrane that remains unknown. We examined the involvement of the mito-KATP channel and the mPTP in the PostC mechanism. Ischemic PostC consisted of three cycles of 15 s reperfusion and 15 s re-ischemia, and was started 30 s after the 7.5 min ischemic load. We recorded N-methyl-d-aspartate receptors (NMDAR)-mediated currents and measured cytosolic Ca2+ concentrations, and mitochondrial membrane potentials in mouse hippocampal pyramidal neurons. Both ischemic PostC and the application of a mito-KATP channel opener, diazoxide, reduced NMDAR-mediated currents, and suppressed cytosolic Ca2+ elevations during the early reperfusion period. An mPTP blocker, cyclosporine A, abolished the reducing effect of PostC on NMDAR currents. Furthermore, both ischemic PostC and the application of diazoxide potentiated the depolarization of the mitochondrial membrane potential. These results indicate that ischemic PostC suppresses Ca2+ influx into the cytoplasm by reducing NMDAR-mediated currents through mPTP opening. The present study suggests that depolarization of the mitochondrial membrane potential by opening of the mito-KATP channel is essential to the mechanism of PostC in neuroprotection against anoxic injury. 相似文献
8.
Here we report effect of ischemia-reperfusion on mitochondrial Ca 2+ uptake and activity of complexes I and IV in rat hippocampus. By performing 4-vessel occlusion model of global brain ischemia,
we observed that 15 min ischemia led to significant decrease of mitochondrial capacity to accumulate Ca 2+ to 80.8% of control whereas rate of Ca 2+ uptake was not significantly changed. Reperfusion did not significantly change mitochondrial Ca 2+ transport. Ischemia induced progressive inhibition of complex I, affecting final electron transfer to decylubiquinone. Minimal
activity of complex I was observed 24 h after ischemia (63% of control). Inhibition of complex IV activity to 80.6% of control
was observed 1 h after ischemia. To explain the discrepancy between impact of ischemia on rate of Ca 2+ uptake and activities of both complexes, we performed titration experiments to study relationship between inhibition of particular
complex and generation of mitochondrial transmembrane potential (ΔΨ m). Generation of a threshold curves showed that complex I and IV activities must be decreased by approximately 40, and 60%,
respectively, before significant decline in ΔΨ m was documented. Thus, mitochondrial Ca 2+ uptake was not significantly affected by ischemia-reperfusion, apparently due to excess capacity of the complexes I and IV.
Inhibition of complex I is favourable of reactive oxygen species (ROS) generation. Maximal oxidative modification of membrane
proteins was documented 1 h after ischemia. Although enhanced formation of ROS might contribute to neuronal injury, depressed
activities of complex I and IV together with unaltered rate of Ca 2+ uptake are conditions favourable of initiation of other cell degenerative pathways like opening of mitochondrial permeability
transition pore or apoptosis initiation, and might represent important mechanism of ischemic damage to neurones. 相似文献
9.
Mitochondrial superoxide flashes reflect a quantal, bursting mode of reactive oxygen species (ROS) production that arises from stochastic, transient opening of the mitochondrial permeability transition pore (mPTP) in many types of cells and in living animals. However, the regulatory mechanisms and the exact nature of the flash-coupled mPTP remain poorly understood. Here we demonstrate a profound synergistic effect between mitochondrial Ca 2+ uniport and elevated basal ROS production in triggering superoxide flashes in intact cells. Hyperosmotic stress potently augmented the flash activity while simultaneously elevating mitochondrial Ca 2+ and ROS. Blocking mitochondrial Ca 2+ transport by knockdown of MICU1 or MCU, newly identified components of the mitochondrial Ca 2+ uniporter, or scavenging mitochondrial basal ROS markedly diminished the flash response. More importantly, whereas elevating Ca 2+ or ROS production alone was inefficacious in triggering the flashes, concurrent physiological Ca 2+ and ROS elevation served as the most powerful flash activator, increasing the flash incidence by an order of magnitude. Functionally, superoxide flashes in response to hyperosmotic stress participated in the activation of JNK and p38. Thus, physiological levels of mitochondrial Ca 2+ and ROS synergistically regulate stochastic mPTP opening and quantal ROS production in intact cells, marking the flash as a coincidence detector of mitochondrial Ca 2+ and ROS signals. 相似文献
10.
Dysregulation of O-GlcNAc modification catalyzed by O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) contributes to the etiology of chronic diseases of aging, including cancer, cardiovascular disease, type 2 diabetes, and Alzheimer's disease. Here we found that natural aging in wild-type mice was marked by a decrease in OGA and OGT protein levels and an increase in O-GlcNAcylation in various tissues. Genetic disruption of OGA resulted in constitutively elevated O-GlcNAcylation in embryos and led to neonatal lethality with developmental delay. Importantly, we observed that serum-stimulated cell cycle entry induced increased O-GlcNAcylation and decreased its level after release from G2/M arrest, indicating that O-GlcNAc cycling by OGT and OGA is required for precise cell cycle control. Constitutively, elevated O-GlcNAcylation by OGA disruption impaired cell proliferation and resulted in mitotic defects with downregulation of mitotic regulators. OGA loss led to mitotic defects including cytokinesis failure and binucleation, increased lagging chromosomes, and micronuclei formation. These findings suggest an important role for O-GlcNAc cycling by OGA in embryonic development and the regulation of the maintenance of genomic stability linked to the aging process. 相似文献
11.
In order to explore the role of mitochondria in proliferation promotion and/or apoptosis induction of lanthanum, the mutual
influences between La 3+ and Ca 2+ on mitochondrial permeability transition pore (PTP) opening were investigated with isolated mitochondria from rat liver.
The experimental results revealed that La 3+ influence the state of mitochondria in a concentration-dependent biphasic manner. La 3+ in nanomolar concentrations, acting as a Ca 2+ analog, entered mitochondrial matrix via the RuR sensitive Ca 2+ channel and elevated ROS level, leading to opening of PTP indicated by mitochondrial swelling, reduction of ΔΨ m and cytochrome c release. Inhibition of PTP with 10 μM CsA attenuated the effects of La 3+. However, micromolar concentrations La 3+ acted mainly as a Ca 2+ antagonist, inhibiting PTP opening induced by Ca 2+. We postulated that this action of La 3+ on mitochondria through interaction with Ca 2+ might be involved in the proliferation-promoting and apoptosis induction by La 3+. 相似文献
12.
O-GlcNAcylation is a common posttranslational modification of nucleocytoplasmic proteins by β-N-acetylglucosamine (GlcNAc). The dynamic addition and removal of O-GlcNAc groups to and from proteins are catalyzed by O-linked N-acetylglucosamine transferase (O-GlcNAc transferase, OGT) and β-N-acetylglucosaminidase (O-GlcNAcase, OGA), respectively. O-GlcNAcylation often modulates protein phosphorylation and regulates several cellular signaling and functions, especially in the brain. However, its developmental regulation is not well known. Here, we studied protein O-GlcNAcylation, OGT, and OGA in the rat brain at various ages from embryonic day 15 to the age of 2 years. We found a gradual decline of global protein O-GlcNAcylation during developmental stages and adulthood. This decline correlated positively to the total protein phosphorylation at serine residues, but not at threonine residues. The expression of OGT and OGA isoforms was regulated differently at various ages. Immunohistochemical studies revealed ubiquitous distribution of O-GlcNAcylation at all ages. Strong immunostaining of O-GlcNAc, OGT, and OGA was observed mostly in neuronal cell bodies and processes, further suggesting the role of O-GlcNAc modification of neuronal proteins in the brain. These studies provide fundamental knowledge of age-dependent protein modification by O-GlcNAc and will help guide future studies on the role of O-GlcNAcylation in the mammalian brain. 相似文献
13.
The metabolite euplotin C (EC), isolated from the marine ciliate Euplotes crassus, is a powerful cytotoxic and pro-apoptotic agent in tumour cell lines. For instance, EC induces the rapid depletion of ryanodine
Ca 2+ stores, the release of cytochrome c from the mitochondria, and the activation of caspase-3, leading to apoptosis. The purpose of this study was to gain further
insight into the mechanisms of EC-induced apoptosis in rat pheochromocytoma PC12 cells. We found that EC increases Bax/Bcl-2
ratio and that Bax is responsible of the EC-induced dissipation of the mitochondrial membrane potential (Δψ m). In addition, EC induces the generation of reactive oxygene species (ROS) without involvement of p53. The inhibition of
ROS generation prevents, at least in part, the pro-apoptotic effects of EC as well as the effects of EC on Bax, Δψ m and intracellular free Ca 2+, indicating a cross-talk between different pathways. However, definition of the effector cascade turns out to be more complex
than expected and caspase-independent mechanisms, acting in parallel with caspases, should also be considered. Among them,
EC increases the expression/activity of calpains downstream of ROS generation, although calpains seem to exert protective
effects.
D. Cervia and M. Garcia-Gil equally contributed to the work. 相似文献
14.
Characteristics for the up-regulated response in the concentration of intracellular calcium ion ([Ca 2+]
i
) and in the sodium ion (Na +) current by serotonin (5-HT) were investigated in differentiated neuroblastoma × glioma hybrid NG108-15 (NG) cells. The results
for the changes in [Ca 2+]
i
by 5-HT were as follows, (1) The 5-HT-induced Ca 2+ response was inhibited by 3 × 10 −9 M tropisetron (a 5-HT 3 receptor blocker), but not by other types of 5-HT receptor blockers; (2) The 5-HT-induced Ca 2+ response was mainly inhibited by calciseptine (a L-type Ca 2+ blocker), but not by other types of Ca 2+ channel blockers or 10 −7 M TTX (a voltage-sensitive Na + channel blocker); (3) When the extracellular Na + was removed by exchange with choline chloride or N-methyl- d-glucamine, the 5-HT-induced Ca 2+ response was extremely inhibited. The results for the 5-HT-induced Na + current by the whole cell patch-clamp technique were as follows, (1) The 5-HT-induced Na + current in differentiated cells was significantly larger than that in undifferentiated cells; (2) The ED 50 value for 5-HT-induced Na + current in undifferentiated and differentiated cells was almost the same, about 4 × 10 −6 M each other; (3) The 5-HT-induced Na + current was completely blocked by 3 × 10 −9 M tropisetron, but not by other 5-HT receptor antagonists and 10 −7 M TTX. These results suggested that 5-HT-induced Ca 2+ response in differentiated NG cells was mainly due to L-type voltage-gated Ca 2+ channels allowing extracellular Na + to enter via 5-HT 3 receptors, but not through voltage-gated Na + channels. 相似文献
15.
Globular adiponectin (gAd) induces the generation of reactive oxygen species (ROS) and nitric oxide (NO) in the murine macrophage cell line RAW 264. We investigated the role of Ca 2+ in gAd-induced ROS and NO generation. Pretreatment with BAPTA-AM, a selective chelator of intracellular Ca 2+ ([Ca 2+] i), partially reduced gAd-induced generation of ROS and NO in gAd-treated RAW 264 cells. The lowest [Ca 2+] i occurred 30 min after gAd treatment, after which [Ca 2+] i increased continually and exceeded the initial level. The mitochondrial Ca 2+ ([Ca 2+] m) detected by Rhod-2 fluorescence started to increase at 6 h after gAd treatment. Pretreatment with a NAD(P)H oxidase inhibitor, diphenyleneiodonium, prevented the reduction of [Ca 2+] i in the early phase after gAd treatment. Calcium depletion by BAPTA-AM had no effect on the gAd-induced [Ca 2+] m oscillation. The administration of a specific calmodulin inhibitor, calmidazolium, significantly suppressed gAd-induced ROS and NO generation and NOS activity. 相似文献
16.
Pomacea (Ampullariidae) snails, commonly referred to as apple snails, serve as prey for many freshwater-dependent predators, and
some species are highly invasive. Identifying limits to apple snail distribution and abundance are pertinent to understanding
their ecology. Calcium (Ca 2+) availability and pH generally influences freshwater snail populations, yet scant data exist for Pomacea snails. We measured 6-week change in shell length (ΔSL) in P. paludosa in two laboratory experiments with varying Ca 2+ and pH levels. ΔSL was significantly higher in ≥28 mg Ca 2+/l compared with treatments ≤14 mg/l. Snails from populations living in low Ca 2+/pH waters did not appear genetically predisposed at growing faster in these conditions. Smallest ΔSL was in snails treated
with 3.6 mg Ca 2+/l and pH < 6.5 water; these snails had signs of shell erosion. Shell crush weights (CWs) were lowest for snails grown in
the lowest Ca 2+/pH treatment. Smaller shells and lower CWs have implications for predation vulnerability and reproductive success. Our results
are consistent with reports associating relatively low snail densities with relatively low Ca 2+/pH waters, and they are consistent with the geographic distribution of P. paludosa as related to the underlying water chemistry as influenced by geology. 相似文献
17.
Neuregulin (NRG) plays an important role on the genesis and differentiation of neurons in the dorsal root ganglion (DRG).
Whether NRG-1β regulates Ca 2+ homeostasis and apoptosis of cultured DRG neurons with excitotoxicity induced by Glu remains unknown. In this study, primary
cultured DRG neurons were used to determine the effects of NRG-1β on Ca 2+ overload and apoptosis of DRG sensory neurons with excitotoxicity induced by Glu. The primary cultured DRG neurons at 48 h
of culture age were then exposed to Glu (0.2 mmol/l), Glu (0.2 mmol/l) plus NRG-1β (20 nmol/l), or Glu (0.2 mmol/l) plus NRG-1β
(20 nmol/l) and phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 (10 μmol/l) for additional 12 h. After that, intracellular
Ca 2+ concentration ([Ca 2+] i) in isolated DRG neurons using the fluorescent Ca 2+ indicator fluo-3 was measured by confocal laser scanning microscope. Apoptotic neurons were monitored by Hoechst 33342 staining.
Expression of caspase-3, procaspase-3, and pAkt was detected by Western blot assay. Administration of 0.2 mmol/l Glu evoked
an increase in [Ca 2+] i, confirming the excitatory effect of Glu. Compared with the control group, apoptotic (condensed and fragmented nuclei) neurons
were observed in Glu-treated cells after Hoechst 33342 staining. The increase caspase-3 of and decrease of procaspase-3 expression
levels after administration of 0.2 mmol/l Glu suggested the apoptotic effects of Glu. These effects could be inhibited by
the presence of NRG-1β. The effects of NRG-1β could be blocked by PI3K inhibitor LY294002. These results implicated that NRG-1β
could prevents Ca 2+ overload and apoptosis by activating PI3K/Akt pathway of primary cultured DRG neurons with excitotoxicity induced by Glu. 相似文献
18.
Crustaceans present a very interesting model system to study the process of calcification and calcium (Ca 2+) transport because of molting-related events and the deposition of CaCO 3 in the new exoskeleton. Dilocarcinus pagei, a freshwater crab endemic to Brazil, was studied to understand Ca 2+ transport in whole gill cells using a fluorescent probe. Cells were dissociated, all of the gill cell types were loaded with
fluo-3 and intracellular Ca 2+ change was monitored by adding Ca as CaCl 2 (0, 0.1, 0.25, 0.50, 1.0 and 5 mM), with a series of different inhibitors. For control gill cells, Ca 2+ transport followed Michaelis–Menten kinetics with K
m = 0.42 ± 0.04 mM and V
max = 0.50 ± 0.02 μM (Ca 2+ change × initial intracellular Ca −1 × 180 s −1; N = 14, r
2 = 0.99). Verapamil (a Ca 2+ channel inhibitor) and amiloride (a Na +/Ca 2+ exchanger [NCX] inhibitor) completely reduced intracellular Ca 2+ transport, while nifedipine, another Ca 2+ channel inhibitor, did not. Vanadate, a plasma membrane Ca 2+-ATPase inhibitor (PMCA), increased intracellular Ca 2+ in gill cells through a decrease in the efflux of Ca 2+. Ouabain increased intracellular Ca 2+, similar to the effect of KB-R, a specific NCX inhibitor for Ca 2+ in the influx mode. Alterations in extracellular [Na] in the saline did not affect intracellular Ca 2+ transport. Caffeine, responsible for inducing Ca release from sarcoplasmic reticulum in vertebrate muscle, increased intracellular
Ca 2+ compared to control, suggesting an effect of this inhibitor in gill epithelial cells of Dilocarcinus pagei, probably through release of intracellular stores. We also demonstrate here that intracellular Ca 2+ in gill cells of Dilocarcinus pagei was kept relatively constant in face of an extracellular Ca concentration of 50-fold, suggesting that crustaceans are able
to display Ca 2+ homeostasis through various Ca 2+ intracellular sequestration mechanisms and/or plasma membrane Ca 2+ influx and outflux that are highly regulatory. In summary, studies using whole gill cells are an interesting approach for
working with real regulatory Ca 2+ mechanisms in intact cells under physiological Ca levels (mM range), compared to earlier work using isolated vesicles of
various epithelial cells. 相似文献
19.
Potassium is taken up by maize ( Zea mays L .) coleoptile cells via a typical plant inward rectifier (K
ir
). Sufficient conductance of this channel is essential in order to maintain auxin-stimulated cell elongation. It was therefore
investigated whether the activity of this channel is subject to direct or indirect control by this growth hormone. Patch-clamp
measurements of whole coleoptile protoplasts revealed no appreciable effect of externally applied 10 μM or 100 μM α-naphthaleneacetic
acid (NAA) on the activity of K
ir
over test periods of ≥ 18 or ≥ 8 min, respectively. When, however, K
ir
was recorded in the cell-attached configiuration and 10 μM NAA administered to the bath medium, the conductance of K
ir
increased significantly in 13 out of 18 protoplasts over the control. This rise occurred at a fixed protoplast voltage after
a lag period of less than 10 min and exhibited no voltage dependency. The absence of response to NAA of protoplasts in the
whole-cell configuration indicates that auxin perception and channel control is linked via a soluble cytoplasmic factor and
that this mediator is washed out or modified upon perfusion of the cytoplasm with pipette solution. To search for this expected
diffusible factor the K
ir
current was recorded before and after elevation of Ca 2+ and H + in the cytoplasm. In the whole-cell configuration the increase in Ca 2+ from a nanomolar value to >1 μM by means of Ca 2+-release from the caged precursor Na 2-DM-nitrophen left K
ir
unaffected. The whole-cell K
ir
conductance was also not affected upon addition of 10 mM Na +-acetate to the bath medium, an operation used to lower the cytoplasmic pH. This excludes a primary role for the known auxin-evoked
rise in cytoplasmic Ca 2+ and H + in K
ir
activity. We postulate that another, as yet unknown, mechanism mediates the auxin-evoked stimulation of the number of active
K
ir
channels in the plasma membrane.
Received: 13 May 1998 / Accepted: 9 November 1998 相似文献
20.
Low voltage-activated, rapidly inactivating T-type Ca 2+ channels are found in a variety of cells, where they regulate electrical activity and Ca 2+ entry. In whole-cell patch-clamp recordings from mouse spermatogenic cells, trace element copper (Cu 2+) inhibited T-type Ca 2+ current ( I
T-Ca) with IC 50 of 12.06 μM. Inhibition of I
T-Ca by Cu 2+ was concentration-dependent and mildly voltage-dependent. When voltage stepped to −20 m V, Cu 2+ (10 μM) inhibited I
T-Ca by 49.6 ± 4.1%. Inhibition of I
T-Ca by Cu 2+ was accompanied by a shift of −2.23 m V in the voltage dependence of steady-state inactivation. Cu 2+ upshifted the current–voltage ( I- V) curve. To know the change of the gating kinetics of T-type Ca 2+ channels, we analyzed the effect of Cu 2+ on activation, inactivation, deactivation and reactivation of T-type Ca 2+ channels. Since T-type Ca 2+ channels are a key component in capacitation and the acrosome reaction, our data suggest that Cu 2+ can affect male reproductive function through T-type Ca 2+ channels as a preconception contraceptive material. 相似文献
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