Extremely low frequency electromagnetic radiation enhanced energy metabolism and induced oxidative stress in Caenorhabditis elegans / 生理学报

The aim of this study was to determine the effects of extremely low frequency electromagnetic field (ELF-EMF) on energy metabolism and oxidative stress in Caenorhabditis elegans (C. elegans). Worms in three adult stages (young adult stage, egg-laying stage and peak egg-laying stage) were investigated under 50 Hz, 3 mT ELF-EMF exposure. ATP levels, ATP synthase activity in vivo, reactive oxygen species (ROS) content, and changes of total antioxidant capacity (TAC) were detected, and worms' oxidative stress responses were also evaluated under ELF-EMF exposure. The results showed that ATP levels were significantly increased under this ELF-EMF exposure, and mitochondrial ATP synthase activity was upregulated simultaneously. In young adult stage, worms' ROS level was significantly elevated, together with upregulated TAC but with a decreased ROS-TAC score indicated by principal component analysis. ROS level and TAC of worms had no significant changes in egg-laying and peak egg-laying stages. Based on these results, we concluded that ELF-EMF can enhance worm energy metabolism and elicit oxidative stress, mainly manifesting as ATP and ROS level elevation together with ATP synthase upregulation and ROS-TAC score decrease in young adult C. elegans.

Action of Mitochondrial Substrates on Neuronal Excitability in Rat Substantia Gelatinosa Neurons

Recent studies indicate that mitochondria are an important source of reactive oxygen species (ROS) in the spinal dorsal horn. In our previous study, application of malate, a mitochondrial electron transport complex I substrate, induced a membrane depolarization, which was inhibited by pretreatment with ROS scavengers. In the present study, we used patch clamp recording in the substantia geletinosa (SG) neurons of spinal slices, to investigate the cellular mechanism of mitochondrial ROS on neuronal excitability. DNQX (an AMPA receptor antagonist) and AP5 (an NMDA receptor antagonist) decreased the malate-induced depolarization. In an external calcium free solution and addition of tetrodotoxin (TTX) for blockade of synaptic transmission, the malateinduced depolarization remained unchanged. In the presence of DNQX, AP5 and AP3 (a group I metabotropic glutamate receptor (mGluR) antagonist), glutamate depolarized the membrane potential, which was suppressed by PBN. However, oligomycin (a mitochondrial ATP synthase inhibitor) or PPADS (a P2 receptor inhibitor) did not affect the substrates-induced depolarization. These results suggest that mitochondrial substrate-induced ROS in SG neuron directly acts on the postsynaptic neuron, therefore increasing the ion influx via glutamate receptors.

A Mitochondrial DNA A8701G Mutation Associated with Maternally Inherited Hypertension and Dilated Cardiomyopathy in a Chinese Pedigree of a Consanguineous Marriage / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Cardiovascular diseases, including dilated cardiomyopathy (DCM) and hypertension, are the leading cause of death worldwide. The role of mitochondrial DNA (mtDNA) in the pathogenesis of these diseases has not been completely clarified. In this study, we evaluate whether A8701G mutation is associated with maternally inherited hypertension and DCM in a Chinese pedigree of a consanguineous marriage.</p><p><b>METHODS</b>Fourteen subjects in a three-generation Han Chinese family with hypertension and DCM, in which consanguineous marriage was present in the parental generation, were interviewed. We divided all the family members into case (7 maternal members) and control group (7 nonmaternal members) for comparison. Clinical evaluations and sequence analysis of mtDNA were obtained from all participants. Frequency differences between maternal and nonmaternal members were tested to locate the disease-associated mutations.</p><p><b>RESULTS</b>The majority of the family members presented with a maternal inheritance of hypertension and DCM. Sequence analysis of mtDNA in this pedigree identified eight mtDNA mutations. Among the mutations identified, there was only one significant mutation: A8701G (P = 0.005), which is a homoplasmic mitochondrial missense mutation in all the matrilineal relatives. There was no clear evidence for any synergistic effects between A8701G and other mutations.</p><p><b>CONCLUSIONS</b>A8701G mutation may act as an inherited risk factor for the matrilineal transmission of hypertension and DCM in conjunction with genetic disorders caused by consanguineous marriage.</p>

A novel mutation T8821G in mitochondrial DNA may be associated with Leber's hereditary optic neuropathy / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To report on clinical, genetic and molecular characterization of two Chinese families with Leber's hereditary optic neuropathy.</p><p><b>METHODS</b>Ophthalmological examinations have revealed variable severity and age at onset of visual loss among the probands and other matrilineal relatives of both families. The entire mitochondrial genome of the two probands was amplified with PCR in 24 overlapping fragments using sets of oligonucleotide primers.</p><p><b>RESULTS</b>The ophthalmological examinations showed that penetrance was 12.5% and 30.0% respectively in the two families. Sequence analysis of the complete mitochondrial genomes in these pedigrees has identified unreported homoplasmic T8821G mutation in the ATPase 6 gene and distinct sets of polymorphisms belonging to haplogroups M10a. The T8821G mutation has occurred at the extremely conserved nucleotide (conventional position 99) of the ATPase6. Thus, this mutation may alter structural formation of ATPase6, thereby leading to failure in the synthesis of ATP involved in visual impairment.</p><p><b>CONCLUSION</b>Above observations have suggested that the ATPase6 T8821G mutation may be involved in the pathogenesis of optic neuropathy in these families.</p>

Investigation of trichloroethylene-induced effects on subcellular proteomes in L-02 hepatic cells / 中华预防医学杂志

<p><b>OBJECTIVE</b>To put the insight into the trichloroethylene (TCE)-induced effect on the differential expression of subcellular proteins in human normal liver cell line (L-02).</p><p><b>METHODS</b>The membrane proteins and nuclear proteins of TCE-treated (8.0 mmol/L) group and controls were extracted by subcellular proteome extraction kit, respectively. The TCE-induced differentially expressions were analyzed by a two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) and matrix-assisted laser desorption/ionization tandem time-of-flight spectrometry (MALDI-TOF-MS). Bioinformatics analysis was used to reveal the biological processes and predict transmembrane domains of differential expressed proteins. The expression of ATP synthase subunit beta (ATP5B), heterogeneous nuclear ribonucleoprotein H2 (hnRNP H2) and far up steam element-binding protein 1 (FUBP1) were measured under TCE treatment by Western blot.</p><p><b>RESULTS</b>After TCE treatment for 24 h in L-02 cells, 14 membrane proteins and 18 nuclear proteins were identified as differential expression. After treated with TCE in concentrations of 0, 2.0, 4.0 and 8.0 mmol/L for 24 h, the relative levels of ATP5B expression were 1.00±0.03, 1.21±0.14, 1.25±0.12 and 1.48±0.17 (F = 8.51, P = 0.007), the relative levels of hnRNP H2 expression were 1.00±0.09, 1.22±0.15, 1.43±0.21, 1.53±0.17 (F = 6.57, P = 0.015), respectively; the relative levels of FUBP1 expression were 1.00±0.11, 0.91±0.07, 0.73±0.04 and 0.67±0.03 (F = 15.81, P = 0.001), respectively, which were consistent with the results in proteomics. The bioinformatics analysis showed that the most dominant biological process were involved in RNA processing (10 proteins, P = 2.46×10(-6)), especially in RNA splicing (9 proteins, P = 1.77×10(-7)).</p><p><b>CONCLUSION</b>The exposure of TCE could alter the expression of membrane proteins and nuclear proteins in L-02 cells. These abnormal expressed proteins involved in RNA splicing would provide novel clues for further understanding of TCE-induced hepatotoxicity.</p>

How does transmembrane electrochemical potential drive the rotation of Fo motor in an ATP synthase?

While the field of ATP synthase research has a long history filled with landmark discoveries, recent structural works provide us with important insights into the mechanisms that links the proton movement with the rotation of the Fo motor. Here, we propose a mechanism of unidirectional rotation of the Fo complex, which is in agreement with these new structural insights as well as our more general ΔΨ-driving hypothesis of membrane proteins: A proton path in the rotor-stator interface is formed dynamically in concert with the rotation of the Fo rotor. The trajectory of the proton viewed in the reference system of the rotor (R-path) must lag behind that of the stator (S-path). The proton moves from a higher energy site to a lower site following both trajectories simultaneously. The two trajectories meet each other at the transient proton-binding site, resulting in a relative rotation between the rotor and stator. The kinetic energy of protons gained from ΔΨ is transferred to the c-ring as the protons are captured sequentially by the binding sites along the proton path, thus driving the unidirectional rotation of the c-ring. Our ΔΨ-driving hypothesis on Fo motor is an attempt to unveil the robust mechanism of energy conversion in the highly conserved, ubiquitously expressed rotary ATP synthases.

Research on relevance between mitochondrial ATP synthase and malignant tumor / 生物医学工程学杂志

Mitochondrial adenosine triphosphate (ATP) synthase is the key enzyme of mitochondrial oxidative phosphorylation reaction. The down-regulation of the mitochondrial ATP synthase is a hallmark of most human carcinomas, which is the embodiment of the bioenergetic signature of cancer in the performance of the decreased oxidative phosphorylation and increased aerobic glycolysis. Combining with the bioenergetic signature of cancer, studies showed that mitochondrial ATP synthase and multidrug resistance and adverse prognosis of tumor were closely related. Its mechanisms are related to post-transcriptional regulation of the ATP synthase, the hypermethylation of the ATP synthase gene and the inhibitor peptide of the mitochondrial ATP synthase, called ATP synthase inhibitory factor 1 (IF1). In this review, we stress the biological characteristics of mitochondrial ATP synthase and the relationship between ATP synthase and multidrug resistance and prognosis of Malignant tumor, in order to find a new way for tumor therapy.

Effects of electroacupuncture with manifestation-root acupoint combination on ultrastructure and biosynthesis in mitochondrial of quadriceps femoris in rats with insulin resistance / 中国针灸

<p><b>OBJECTIVE</b>To explore the mechanism of electroacupuncture on improving insulin resistance of rat from aspects of morphology and function of mitochondrial in quadriceps femoris.</p><p><b>METHODS</b>Forty-eight 8-week Wistar rats (female and male in half) were randomly divided into a normal group (16 rats, group A), a model control group (16 rats, group B), a model plus electroacupuncture (EA) group (8 rats, group C) and a model plus sham acupoint EA group (8 rats, group D). Group A was given with basic diet while high-fat diet was applied in the group B, group C and group D for 8 weeks to establish model of insulin resistance. After the model establishment, "Guanyuan" (CV 4), "Zhongwan" (CV 12), "Zusanli" (ST 36) and "Fenglong" (ST 30) were selected according to acupoint combination of manifestation-root in the group C, while four points in non-meridian area where 1 to 2 mm next to the acupoints used in group C were selected in the group D. The treatment was given 15 min per time with 1 mA of intensity and 2 Hz in frequency, 5 times per week for totally 8 weeks. The transmission electron microscope was adopted to observe mitochondria structure, and chemical colorimetry was used to test the activity of adenosine triphosphate (ATP) synthase and phosphomolybdic acid colorimetry was applied to measure the content of ATP.</p><p><b>RESULTS</b>After the treatment, the body mass was (401.63 +/- 109.81) g in the group B, which was significantly higher than (305.88 +/- 62.72) g in the group A (P < 0.05); morphological structure of mitochondrion was damaged, showing swelling and deformation; the activity of ATP synthase was decreased (P < 0.05) and the content of ATP in tissue of quadriceps femoris was also obviously lowered (P < 0.05). The body mass was (294.13 +/- 53.78) g in the group C, which was significantly lower than that in the group B (P < 0.05); the damaged mitochondrion was restored and merged among each other; the activity of ATP synthase was increased (P < 0.05); the content of ATP in tissue of quadriceps femoris was obviously lifted (P < 0.05). The results in group D were not different from those in group B.</p><p><b>CONCLUSION</b>The electroacupuncture with manifestation-root acupoint combination could improve the recovery of damaged structure of mitochondrion and promote the merge among each other, which could enhance oxidizing capacity, lower body mass and improve synthetic rate of ATP.</p>

Mitochondrial disorders associated with mitochondrial respiratory chain complex V deficiency / 中国当代儿科杂志

The mammalian mitochondrial ATP synthase, also as known as mitochondrial respiratory chain complex V, is a large protein complex located in the mitochondrial inner membrane, where it catalyzes ATP synthesis from ADP, Pi, and Mg2+ at the expense of an electrochemical gradient of protons generated by the electron transport chain. Complex V is composed of 2 functional domains F0 and F1. The clinical features of patients are significantly heterogeneous depending on the involved organs. Most patients with complex V deficiency had clinical onset in the neonatal period with severe brain damage or multi-organ failure resulting in a high mortality. Neuromuscular disorders, cardiomyopathy, lactic acidosis and 3-methylglutaconic aciduria are common findings. Complex V consists of 16 subunits encoded by both mitochondrial DNA and nuclear DNA. On MT-ATP6, MT-ATP8, ATPAF2, TMEM70 and ATP5E gene of mitochondrial DNA, many mutations associated with Complex V deficiency have been identified. Here, the pathology, clinical features, diagnosis, treatment and molecular genetics of Complex V deficiency were summarized.

Investigation of the mitochondrial ATPase 6/8 and tRNALys genes mutations in Autism

Autism results from developmental factors that affect many or all functional brain systems. Brain is one of tissues which are crucially in need of adenosine triphos-phate [ATP]. Autism is noticeably affected by mitochondrial dysfunction which impairs energy metabolism. Considering mutations within ATPase 6, ATPase 8 and tRNALys genes, associated with different neural diseases, and the main role of ATPase 6/8 in energy generation, we decided to investigate mutations on these mtDNA-encoded genes to reveal their roles in autism pathogenesis. In this experimental study, mutation analysis for the mentioned genes were performed in a cohort of 24 unrelated patients with idiopathic autism by employing amplicon sequencing of mtDNA fragments. In this study, 12 patients [50%] showed point mutations that represent a significant correlation between autism and mtDNA variations. Most of the identified substitutions [55.55%] were observed on MT-ATP6, altering some conserved amino acids to other ones which could potentially affect ATPase 6 function. Mutations causing amino acid replacement denote involvement of mtDNA genes, especially ATPase 6 in autism pathogenesis. MtDNA mutations in relation with autism could be remarkable to realize an understandable mechanism of pathogenesis in order to achieve therapeutic solutions

Effects of electrode on epileptogenic focus potential and expressions of the beta subunit of ATP synthase in rats with penicillin-induced epilepsy / 生物医学工程学杂志

The changed process of bioenergy and the effects of electrode interfering on penicillin-induced epileptic brains in epileptic seizures rats were investigated. Fifty Sprague-Dawley (SD) rats were randomly divided into 4 groups, i. e. normal saline control group (group A), penicillin model group (group B), metal electrode interfere group (group C) and insulated electrode interfere group (group D). The epileptogenic potential and the expressions of the beta subunit of-ATP synthase( ATP5B) in hippocampal neurons were measured. The epileptogenic foucus potential and expressions of ATP5B in hippocampus neurons showed that the trend increased at first and decreased implantation of later, and the implantation of metal electrodes decreased the epileptogenic foucus potential at corresponding time point, but had no effect on the expressions of ATP5B. The change of epileptogenic focus potential was reduced by implantation of metal electrode, possibly due to the alteration of corrosponding bioenergy metabolism which had participated in the process of epileptic seizure.

Effect of safflor yellow B on vascular endothelial cells injury induced by angiotensin-II / 药学学报

This study is to investigate protective effect of safflor yellow B (SYB) against vascular endothelial cells (VECs) injury induced by angiotensin-II (Ang-II). VECs were cultured and divided into six groups: control group, Ang-II group, Ang-II + SYB (1 micromolL(-1)) group, Ang-II + SYB (10 micromolL(-1)) group, Ang-II + SYB (100 micromolL(-1)) group and Ang- II + verapamil (10 micromolL(-1)) group. Except control group, all of VECs in other groups were treated with Ang- II at the final concentration of 0.1 micromolL(-1). Mitochondria membrane potential (MMP) and free calcium concentration ([Ca2+]i) were measured by laser scanning confocal microscopy, and mitochondria complex IV activity was detected by BCA method. The levels of reactive oxygen species (ROS) in VECs were analyzed by fluorescence detector and apoptosis of VECs was observed by flow cytometer. Caspase 3 was determined by Western blotting method. Comparing with control group, Ang-II was able to increase [Ca2+]i and ROS level, decrease MMP level, inhibit complex IV activity and enhance caspase 3 activity in VECs, as a result, enhance apoptosis of VECs. But SYB could significantly reduce the result induced by Ang- II relying on different dosages (P < 0.05 or P < 0.01). SYB was able to eliminate the effect of Ang-II on VECs via regulating [Ca2+]i, mitochondrial structure and function and inhibiting apoptosis.

Preparation of monoclonal antibody against lung cancer and identification of its targeting antigen / 生物医学工程学杂志

A mouse-anti-human monoclonal antibody was produced by using the membrane proteins of human lung carcinoma cell line A549 as the immunogen to generate monoclonal antibodies against lung carcinoma with the use of hybridoma techniques. McAb4E7 was prepared successfully. To identify its antigen, proteomic technologies such as two-dimenstional electrophoresis, western blotting and mass spectrometry were employed. The targeting antigen of McAb4E7 expressed positive in human lung cancer cell lines A549 and human hepatocarcinoma cell line HepG2, moreover, the expression of the antigen was stronger in A549 cells. Finally, we obtained one positive protein in A549 cell line that has strong affinity and specificity for McAb4E7, which was identified to be ATP synthase beta subunit. We identified ATP synthase beta subunit as the targeting antigen of lung carcinoma special monoclonal antibody McAb4E7.

Clinicopathologic study of 7 cases of gastric T-cell lymphoma / 中华病理学杂志

<p><b>OBJECTIVE</b>To study the clinicopathologic characteristics of gastric T-cell lymphoma.</p><p><b>METHODS</b>The clinicopathologic features of 7 cases of gastric T-cell lymphoma were retrospectively reviewed. Immunohistochemical study, T-cell receptor gene rearrangement analysis and evaluation of Epstein Barr virus (EBV) status were also performed.</p><p><b>RESULTS</b>The median age at onset of gastric T-cell lymphoma was 45 years. The male-to-female ratio was 6 to 1. The clinical information was available in 6 cases; and one of them had history of persistent diarrhea and 5 had hypoproteinemia. Histologically, 5 cases consisted of large lymphoma cells and the remaining 2 cases showed mainly medium-sized cells. Intraepithelial lymphoma cell infiltration was found in one case. The lymphoma cells of all cases were negative for CD20 and CD79a. CD3 and TIA-1 expression was noted in 6 of the 7 cases. CD5, βF-1 and CD30 were positive in 4 cases and CD4 was positive in 3 cases. In-situ hybridization for Epstein-Barr virus-encoded RNA was negative. Clonal T-cell receptor gene rearrangement was demonstrated in all cases.</p><p><b>CONCLUSION</b>Gastric T-cell lymphoma is a rare type of malignant lymphoma, with distinctive clinicopathologic characteristics.</p>

Effect of rosiglitazone on tumor necrosis factor-alpha-induced nuclear factor-kappaB and coupling factor 6 expressions in human umbilical vein endothelial cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effect of rosiglitazone on the expression of nuclear factor-kappaB (NF-kappaB) and coupling factor 6 (CF6) induced by tumor necrosis factor-alpha (TNF-alpha) in cultured human umbilical vein endothelial cells (HUVEC).</p><p><b>METHODS</b>Cultured HUVEC of passage 3-5 were stimulated with TNF-alpha and then cultured in the presence of rosiglitazone. The expression of CF6 and NF-kappaB subunit p65 were evaluated by immunocytochemistical method.</p><p><b>RESULTS</b>Pretreatment of HUVECs with rosiglitazone inhibited TNF-alpha-induced expression of CF6 in a dose-dependent manner. The activation of CF6 stimulated by TNF-alpha was suppressed by ROS in a dose-dependent manner.</p><p><b>CONCLUSION</b>TNF-alpha-induced enhancement of the gene expression and release of CF6 is mediated by activation of NF-kappaB signaling pathway. ROS can inhibit the activation of IKK, block NF-kappaB signaling pathway and inhibit the expression of CF6, which may be the mechanism underlying the action of TZDs on hypertension.</p>

Mutation of MTCYB and MTATP6 is associated with asthenospermia / 中华男科学杂志

<p><b>OBJECTIVE</b>To explore the correlation of the mutation of MTCYB and MTATP6 genes in sperm mitochondria with asthenospermia.</p><p><b>METHODS</b>We extracted mtDNA from 80 semen samples of asthenospermia and 20 of normal sperm motility, amplified the MTCYB and MTATP6 genes by PCR, and analyzed their mutation by sequencing and BLAST matching.</p><p><b>RESULTS</b>The deletion of both MTCYB and MTATP6 were detected in 20 of the 80 asthenospermia samples, MTCYB deletion in 16 and MTATP6 deletion in 4, accounting for 20% and 5% respectively. Sequencing and BLAST matching revealed G8887A mutation in the MTATP6 gene in the asthenospermia samples, with a mutation rate of 20%, while no regular mutation was noted in MTCYB. Neither significant deletion nor mutation was observed in any of the 20 samples of normal sperm motility.</p><p><b>CONCLUSION</b>Both the deletion and mutation of MTCYB and MTATP6 genes in sperm mitochondria might affect sperm motility in adults.</p>

Extracellular ATP is generated by ATP synthase complex in adipocyte lipid rafts

Mitochondrial biogenesis is known to accompany adipogenesis to complement ATP and acetyl-CoA required for lipogenesis. Here, we demonstrated that mitochondrial proteins such as ATP synthase alpha and beta, and cytochrome c were highly expressed during the 3T3-L1 differentiation into adipocytes. Fully-differentiated adipocytes showed a significant increase of mitochondria under electron microscopy. Analysis by immunofluorescence, cellular fractionation, and surface biotinylation demonstrated the elevated levels of ATP synthase complex found not only in the mitochondria but also on the cell surface (particularly lipid rafts) of adipocytes. High rate of ATP (more than 30 micrometer) synthesis from the added ADP and Pi in the adipocyte media suggests the involvement of the surface ATP synthase complex for the exracellular ATP synthesis. In addition, this ATP synthesis was significantly inhibited in the presence of oligomycin, an ATP synthase inhibitor, and carbonyl cyanide m-chlorophenylhydrazone (CCCP), an ATP synthase uncoupler. Decrease of extracellular ATP synthesis in acidic but not in basic media further indicates that the surface ATP synthase may also be regulated by proton gradient through the plasma membrane.

Effects of chronic intermittent hypoxic exposure on myocardial mitochondria ATPase and enzyme complexes of respiratory chain in rats / 中国应用生理学杂志

<p><b>AIM</b>To study the effects of acute and chronic intermittent hypoxic exposure on the activities of Na+ , K+ -ATPase, Ca2 + , Mg2 + -ATPase of myocardial mitochondria and enzyme complexes of respiratory chain in rats.</p><p><b>METHODS</b>The activities of Na , K+ -ATPase, Ca2+ , Mg2+ -ATPase of myocardial mitochondria and enzyme complexes of respiratory chain were investigated after chronic intermittent hypoxic exposure (3000 m and 5000 m, 4 h/d, 2 w respectively) and normoxic rats were exposed to hypoxia (8000 m) for 4h.</p><p><b>RESULTS</b>(1) Hypoxia had no effects on the activity of Na+, K+ -ATPase in myocardial mitochondria of rats. (2) Compared with normoxic control rats, the activity of Ca2+, Mg2+ -ATPase in myocardial mitochondria of acute hypoxic rats was reduced significantly. After chronic intermittent hypoxic exposure, its activity was increased significantly compared with that of acute hypoxic rats. (3) Compared with normoxic control rats, the activities of enzyme complex I, II and IV of respiratory chain in acute hypoxic rats were reduced significantly. After chronic intermittent hypoxic exposure, their activities were increased significantly compared with those of acute hypoxic rats. Under the same experimental conditions, hypoxia had no effects on the activity of enzyme complex III.</p><p><b>CONCLUSION</b>After chronic intermittent hypoxic exposure, the activities of Na+, K+ -ATPase, Ca2+, Mg2+ -ATPase of myocardial mitochondria and enzyme complexes of respiratory chain were increased significantly. These suggested that chronic intermittent hypoxic exposure could improve the functions of respiratory chain in myocardial mitochondria and keep the normal energy metabolism.</p>

Ovicidal action of quercetin correlated to its effect on mitochondrial ATPase activity

Effects of quercetin [3,5,7,3;4 Pentahyd-roxyflavone] on the hatchability of egg masses of a susceptible strain of Spodonteta littoralis ware studied. There was linear correlation between quercetin concentration and hatchability of eggs s to a concentration of 250 ppm which reduces hatchability to 15%. Isolation and assay for the activity of the mitochondrial ATPase from the treated eggs showed a decrease in the enzyme activity that was associated with the observed effects of quercetin on the egg hatchability. Study of the effects of quercetin on the purified enzyme from untreated eggs showed an inhibition of the enzyme activity with quercetin an I[50] value was determined as of 25 uM for the purified enzyme from 2-days old egg masses. These sresults suggest a possible involvement of egg mitochondrial F1-ATPase in the mode of quercetin effect on egg hatchability