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At least 451 records · Page 25Linked to original sources
PubMed1992

The combined effects of cocaine and amphetamine on primary postnatal rat heart cell cultures.

Recent reports demonstrated that perinatal exposure to cocaine (Coc) and amphetamines (Amph) predisposed the infant to adverse cardiovascular consequences. Dose- and time-dependent effects of Coc and Amph on postnatal rat myocardial cell cultures are described. Contractile activity, morphology, lactate dehydrogenase (LDH) release, MTT formazan production, and neutral red (NR) retention were determined. No contractile activity was observed in cultures treated with the highest drug doses. After 24 h, the percentage of areas exhibiting contractile activity was decreased in cultures exposed to the lowest doses of both drugs. When Coc and Amph were combined, beating rates were significantly altered. Morphologic alterations were observed in all treatment groups. LDH release occurred in cultures exposed to the highest doses of both drugs. No significant differences were observed for MTT or NR. These data demonstrate that Coc and Amph doses > or = 1 x 10(-5) M induce adverse effects on morphology and contractile activity of postnatal myocardial cell cultures.

Amphetamine↗
PubMed1998

Metabolic inhibition potentiates AMPA-induced Ca2+ fluxes and neurotoxicity in rat cerebellar granule cells.

The effects of partial metabolic inhibition (induced by 2 h exposure to low concentrations of cyanide (NaCN)) on the glutamate receptor agonist alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)-induced excitotoxicity and elevation of free cytoplasmic Ca2+ levels ([Ca2+]i) were studied in glucose-deprived primary cultures of cerebellar granule cells. Co-application of AMPA plus NaCN caused a marked increase of cell death, with morphological features of both necrotic and apoptotic cell death as estimated by the capacity of cultured cerebellar granule cells to metabolize 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide into formazan (MTT method), and by measuring the amount of DNA fragmentation in neurons using an ELISA test for histone-bound DNA fragments, respectively. Cell morphology was assessed by confocal microscopy of propidium iodide-stained cultures. No toxic effects were observed when AMPA or a low concentration of NaCN (0.1-0.3 mM; in the presence of NMDA receptor antagonist MK-801; 10 microM) were applied alone. The neurotoxic actions induced by AMPA plus NaCN were preceded and accompanied by a significant elevation of [Ca2+]i, as well as by depletion of neuronal ATP stores. The marked enhancement in the functional responsiveness of AMPA receptors in energetically compromised neurons suggests that at least under certain conditions AMPA receptors may play an important role in excitotoxic processes which might be of relevance for the slowly developing neuronal death seen in several neurodegenerative diseases.

Adenosine Triphosphate↗
PubMed1976

Evaluation of some biological tests as parameters for microbial activities in soils. I. Laboratory experiments.

The experiments were confined to the effects of the addition of different sources of carbon (glucose, wheat straw, and sawdust) on the microbial activities in soils: loamy sand, loam and saline clay were used. The parameters used for this purpose were total bacterial counts, dehydrogenase test, CO2 evolution, and oxidation of organic carbon. Salinity of soils had deleterious effects on all the parameters used. Addition of organic matter resulted in marked increases in bacterial counts, formazan production, and CO2 evolution. Glucose showed the most rapid effect and highest levels. Wheat straw yielded the highest results and sawdust always showed the least effect.

Bacteria↗
PubMed1999

Evaluation of the cytotoxicity of calcium phosphate root canal sealers by MTT assay.

The purpose of this study was to evaluate the cytotoxicity of some calcium phosphate-based sealers (Sankin apatite root canal sealers (SARCS) types 1 to 3) in comparison with currently used sealers (CRCS, Ketac Endo, AH26, and Endomethasone) by using MTT assay on L929 cells. Monolayer cell cultures were prepared on 96-well plates. After incubation at 37 degrees C in a humidified 5% CO2-containing air atmosphere for 24 h in the presence of each sealer extracts, 25 microliters of 5 mg/ml of MTT in saline were added into each well and incubated a further 3 h at 37 degrees C. A solubilization buffer consisting of 23% sodium dodecyl sulfate in 50% N,N-dimethylformamide (pH 4.7) was used to dissolve formazan precipitate. The optical densities of the plates were then read by a microplate spectrophotometer at 570 nm. Greater magnitude of optical density due to intense blue coloring is regarded as showing a higher percentage of cell viability. Among the different types of sealers, SARCS types 1 to 3 and CRCS did not exert any cytotoxic effects, whereas AH26, Ketac Endo, and Endomethasone produced some cytotoxicity.

Animals↗
PubMed2003

Rhodamine B as a mitochondrial probe for measurement and monitoring of mitochondrial membrane potential in drug-sensitive and -resistant cells.

In order to get more insight into the energetic state of multidrug-resistance (MDR) cell compared with its corresponding sensitive cell, a noninvasive fluorescence method for determining and monitoring the mitochondrial membrane potential (DeltaPsi(m)), using rhodamine B and 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) was established. Rhodamine B distributes across biological membranes in response to the electrical transmembrane potential. P-glycoprotein- and MRP1-protein-mediated efflux do not create a concentration gradient, leading the cell-rhodamine B system to reach a steady state, where the ratio of cytosolic to extracellular rhodamine B was equal to 1. The mitochondrial matrix rhodamine B concentration was precisely determined as a decrease of rhodamine B fluorescence in the presence of formazan, a rhodamine B fluorescence quencher, which locally accumulates in the matrix of mitochondria. The kinetics of decrease in rhodamine B fluorescence (V(i)) can be used to estimate DeltaPsi(m) using the Nernst equation: DeltaPsi(m)=-61.54 log V(i)-258.46. The DeltaPsi(m) values determined were -160+/-4 mV for K562 cell, -146+/-6 mV for K562/adr cell, -161+/-10 mV for GLC4 cell and -168+/-2 mV for GLC4/adr cell. An increase or a decrease in DeltaPsi(m) consequently followed an increase or a decrease in the cellular ATP contents. An increase ATP content in the two MDR cell lines can protect cells from cytotoxicity induced by pirarubicin.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1999

Reduction of a tetrazolium salt, CTC, by intact HepG2 human hepatoma cells: subcellular localisation of reducing systems.

Cell-mediated reduction of tetrazolium salts, including MTT, XTT, MTS, NBT, NTV, INT, in the presence or absence of intermediate electron carriers is used as a convenient test for animal or bacterial cell viability. Bioreduction of tetrazolium is considered an alternative to a clonogenic assay and a thymidine incorporation assay. However, correlation between clonogenic potential and capacity to reduce tetrazolium has not been demonstrated convincingly. Moreover, despite a wide use of tetrazolium viability assays, the mechanism and subcellular localisation of reducing systems or species in viable intact cells have not been fully elucidated. We report evidence indicating that a tetrazolium salt CTC can be reduced in the presence as well as in the absence of an electron carrier by viable HepG2 human hepatoma cells. CTC-formazan is formed within or at the outer surface of plasma membranes. We hypothesise that in the presence of an electron carrier the electron donors active in the reduction of CTC are located in the intracellular compartment, as well as in plasma membranes. However, in the absence of an electron carrier, the reduction occurs primarily via a plasma membrane-associated enzymatic system or species.

Carcinoma, Hepatocellular↗
PubMed2000

The use of the tetrazolium salt XTT for the estimation of biological activity of activated sludge cultivated under steady-state and transient regimes.

The tetrazolium salt 3'-¿1-[(phenylamino)-carbonyl]-3, 4-tetrazolium¿-bis (4-methoxy-6-nitro) benzenesulfonic acid hydrate (XTT) was used as a tool for estimating the activity of the electron transport system (ETS) in activated sludge cultivated under steady-state and transient regimes in chemostat culture. Production of formazan by reduction of XTT depended on the initial concentration of the XTT following a saturation law and was proportional to live cell biomass. Addition of cyanide (KCN) to activated sludge gave an initial 1.5-fold increase in XTT reduction, while addition of 3,5-dichlorophenol (3,5-DCP) reduced this value drastically. At steady-state and transient regimes of an activated sludge chemostat, oxygen uptake rate (OUR) and XTT reduction rate were highly correlated and indicated significant variations depending on the growth conditions.

Bacteria↗
PubMed2000

Measurement of cellular 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction activity and lactate dehydrogenase release using MTT.

3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction assay and lactate dehydrogenase (LDH) release assay have been widely used for evaluating cell viability in culture. MTT reduction assay measures the redox activity of living cells, while LDH assay measures the activity of LDH released into the medium from dead cells. In this paper, we introduce a quick and simple method of measuring cellular MTT reduction and LDH release with the same dye, MTT. The substrate mixture for measuring LDH activity contained lactate, beta-nicotinamide adenine dinucleotide, 1-methoxyphenazine methosulfate, MTT and Triton X-100. When the medium containing LDH was mixed with the substrates, MTT was converted into MTT formazan in proportion to LDH activity. This method was successfully applied for evaluating t-butyl hydroperoxide toxicity in cultured rat cortical astrocytes and glutamate toxicity in cultured rat hippocampal neurons. Our method is economical and convenient especially for measuring cellular MTT reduction and LDH release in the same culture.

Animals↗
PubMed1992

Gut-derived substances in activation of hepatic macrophages after partial hepatectomy in rats.

When liver perfusion with nitro blue tetrazolium and phorbol myristate acetate was performed in rats 24 h after two-thirds liver resection, there were marked deposits of formazan converted from nitro blue tetrazolium in hepatic macrophages throughout the liver, indicating macrophage activity. The extent of the deposits was significantly reduced when perfusion was performed following oral administration of polymyxin B sulfate, a non-absorbable bacteriocidal agent against gram-negative bacilli which can also bind endotoxin lipopolysaccharides. Polymyxin B sulfate administration also attenuated the derangements of SGPT and the histological liver injury provoked by endotoxin administration after partial hepatectomy. These results suggests that gut-derived substances sensitive to polymyxin B sulfate may contribute to activation of hepatic macrophages after partial hepatectomy in rats.

Animals↗
PubMed1983

Simple enzymatic detection method for urinary sulfated 7 alpha-hydroxy bile acids in normal subjects and in patients with acute hepatitis.

Urinary sulfated primary bile acids, 7 alpha-hydroxy bile acids, are detected by an enzymatic method using 7 alpha-hydroxysteroid dehydrogenase (EC 1.1.1.-, 7 alpha-HSD) after chromatographic fractionation on Sephadex G-25. Urinary sulfated or glucuronated bile acids are hydrolyzed by beta-glucuronidase/sulfatase (EC 3.2.1.31/EC 3.1.6.1) from Helix pomatia and then released 7 alpha-hydroxy bile acids are detected with 7 alpha-HSD in the presence of beta-ND+, diaphorase (EC 1.6.99.2, from Clostridium kluyveri) and 2-p-iodophenyl-3-p-nitrophenyl-5-phenyltetrazolium chloride. The absorbance of formazan formed during the enzymic reaction is measured at 500 nm. Excretion values of 7 alpha-hydroxy bile acids in normal subjects and in patients with acute hepatitis were compared. This enzymatic detection method for the excretion pattern of urinary 7 alpha-hydroxy bile acids may be useful for clinical diagnosis.

Bile Acids and Salts↗
PubMed2000

Comparison of the effects of bile acids on cell viability and DNA synthesis by rat hepatocytes in primary culture.

Bile acid-induced inhibition of DNA synthesis by the regenerating rat liver in the absence of other manifestation of impairment in liver cell viability has been reported. Because in experiments carried out on in vivo models bile acids are rapidly taken up and secreted into bile, it is difficult to establish steady concentrations to which the hepatocytes are exposed. Thus, in this work, a dose-response study was carried out to investigate the in vitro cytotoxic effect of major unconjugated and tauro- (T) or glyco- (G) conjugated bile acids and to compare this as regards their ability to inhibit DNA synthesis. Viability of hepatocytes in primary culture was measured by Neutral red uptake and formazan formation after 6 h exposure of cells to bile acids. The rate of DNA synthesis was determined by radiolabeled thymidine incorporation into DNA. Incubation of hepatocytes with different bile acid species - cholic acid (CA), deoxycholic acid (DCA), chenodeoxycholic acid (CDCA) and ursodeoxycholic acid (UDCA), in the range of 10-1000 microM - revealed that toxicity was stronger for the unconjugated forms of CDCA and DCA than for CA and UDCA. Conjugation markedly reduced the effects of bile acids on cell viability. By contrast, the ability to inhibit radiolabeled thymidine incorporation into DNA was only slightly lower for taurodeoxycholic acid (TDCA) and glycodeoxycholic acid (GDCA) than for DCA. When the effect of these bile acids on DNA synthesis and cell viability was compared, a clear dissociation was observed. Radiolabeled thymidine incorporation into DNA was significantly decreased (-50%) at TDCA concentrations at which cell viability was not affected. Lack of a cause-effect relationship between both processes was further supported by the fact that well-known hepatoprotective compounds, such as tauroursodeoxycholic acid (TUDCA) and S-adenosylmethionine (SAMe) failed to prevent the effect of bile acids on DNA synthesis. In summary, our results indicate that bile acid-induced reduction of DNA synthesis does not require previous decreases in hepatocyte viability. This suggests the existence of a high sensitivity to bile acids of cellular mechanisms that may affect the rate of DNA repair and/or proliferation, which is of particular interest regarding the role of bile acids in the etiology of certain types of cancer.

Animals↗
PubMed1997

Enterocyte viability and mitochondrial function after graded intestinal ischemia and reperfusion in rats.

Ischemia/reperfusion of the small intestine can lead to metabolic and structural alterations in the mucosa. Cellular dysfunction occurs when mitochondrial metabolism is compromised, which may ultimately lead to impaired organ function. The aims of this study were to assess the suppression of cellular and mitochondrial oxidative metabolism and involvement of mitochondria in the ischemia/reperfusion injury. The mitochondria were prepared from isolated enterocytes obtained from the small intestine of anesthetized adult rats following different time periods of ischemia and ischemia followed by 5 min reperfusion. Cellular and mitochondrial function were assessed using MTT (3-(4,5-Dimethylthiazol-2-yl) -2,5-diphenyl tetrazolium bromide) reduction assay. Ischemia of increasing time periods caused a progressive decrease in cellular and mitochondrial MTT reduction in enterocytes and reperfusion showed further decrease of MTT formazan formation. Inclusion of 1 mM succinate, as respiratory substrate, showed reversal of suppression of mitochondrial function in 30-60 min ischemia whereas 90 min ischemia or short time period ischemia followed by 5 min reperfusion indicated an irreversible damage to mitochondria. This study indicated that mitochondria are a sensitive target of damage due to oxygen deficiency and possibly due to sudden burst of oxygen free radicals. Mitochondria can withstand short periods of ischemia whereas long duration ischemia or reperfusion results in irreversible damage to mitochondrial function.

Animals↗
PubMed2005

Early phase of amyloid beta42-induced cytotoxicity in neuronal cells is associated with vacuole formation and enhancement of exocytosis.

Amyloid beta (Abeta) neurotoxicity is believed to play a critical role in the pathogenesis of Alzheimer's disease (AD) mainly because of its deposition in AD brain and its neuronal toxicity. However, there have been discrepancies in Abeta-induced cytotoxicity studies, depending on the assay methods. Comparative analysis of Abeta42-induced in vitro cytotoxicity might be useful to elucidate the etiological role of Abeta in the pathogenesis of AD. In this study, MTT, CCK-8, calcein-AM/EthD-1 assays as well as thorough microscopic examinations were comparatively performed after Abeta42 treatment in a neuronal precursor cells (NT2) and a somatic cells (EcR293). Extensive formation of vacuoles was observed at the very early stage of Abeta42 treatment in both cells. Early observation of Abeta42 toxicity as seen in vacuole formation was also shown in MTT assay, but not in CCK-8 and calcein-AM/EthD-1 assays. In addition, Abeta42 treatment dramatically accelerated MTT formazan exocytosis, implying its effect on the extensive formation of cytoplasmic vacuoles. Abeta42 seems to cause indirect inhibition on the intracellular MTT reduction as well as vacuole formation and exocytosis enhancement. Following the acute cellular dysfunction induced by Abeta42, the prolonged treatment of micromolar concentration of Abeta42 resulted in slight inhibition on redox and esterase activity. The early Abeta42-induced vacuolated morphology and later chronic cytotoxic effect in neuronal cell might be linked to the chronic neurodegeneration caused by the accumulation of Abeta42 in AD patients' brain.

Amyloid beta-Peptides↗
PubMed2002

MTS colorimetric assay in combination with a live-dead assay for testing encapsulated L929 fibroblasts in alginate poly-L-lysine microcapsules in vitro.

Biomaterials such as applied in microcapsules may have harmful effects on encapsulated cells. Up to now, there are no adequate assays available for testing the function and viability of cells in capsules. Therefore, we investigated whether the combination of MTS proliferation assay and live-dead viability assay is suitable for testing microencapsulated L929 fibroblasts in long-time culture. Proliferation of L929 cells was shown by a significant increase of formazan absorbance within the first 3 weeks (Day 0: 0.132 +/- 0.047; Day 7: 0.404 +/- 0.101; Day 14: 0.728 +/- 0.239; Day 21: 0.877 +/- 0.224) followed by stagnation and decrease thereafter. This was confirmed by an increasing proportion of dead cells measured by the live-dead assay. Thus, proliferation of encapsulated L929 can be reliably investigated by the MTS assay. In combination with life-dead assays, the proliferation can be correlated to the survival rate of the encapsulated cells.

Alginates↗
PubMed2001

alpha1-Adrenoceptors during simulated ischemia and reoxygenation of the human myocardium: effect of the dose and time of administration.

OBJECTIVE: We sought to investigate the effect of alpha1-adrenoceptor activity on the ischemic and reoxygenated human myocardium. METHODS: Right atrial appendages (n = 6 per group) obtained during elective cardiac operations were sliced and stabilized in normoxic normothermic buffer solution for 30 minutes and then subjected to 90 minutes of simulated ischemia, followed by 120 minutes of reoxygenation. In study 1 the dose responses to the alpha1-adrenoceptor agonist phenylephrine (0.01, 0.1, 1, 10, and 100 micromol/L) and to the alpha1-adrenoceptor antagonist prazosin (0.1, 1, 10, and 100 micromol/L) when administered for 10 minutes before ischemia, during ischemia, and during reoxygenation were examined. The influence of the time of administration (ie, before ischemia, during ischemia, or during reoxygenation) of phenylephrine (0.1 micromol/L) and prazosin (10 micromol/L) was then investigated in study 2. In study 3 the effect of the combined administration of phenylephrine given before ischemia and prazosin given during ischemia was investigated. In study 4 the protective effect of phenylephrine given before ischemia (for 10 minutes or for 5 minutes with a 5-minute washout period) was compared with that of ischemic preconditioning (5 minutes of ischemia and 5 minutes of reoxygenation). At the end of each protocol, the leakage of creatine kinase (in units per gram of wet weight) and the reduction of 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide to insoluble formazan dye (in millimoles per gram of wet weight) were measured. RESULTS: Phenylephrine is maximally beneficial at 0.1 and 1 micromol/L (creatinine kinase, 0.97 +/- 0.06 and 0.95 +/- 0.03 U/g, respectively; 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide, 153.0 +/- 7.8 and 156.2 +/- 6.7 mmol/g, respectively) compared with ischemic control (creatine kinase, 1.87 +/- 0.03 U/g; 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide, 108.5 +/- 6.8 mmol/g; P <.05) but prazosin is detrimental at concentrations above 10 micromol/L (creatine kinase, 5.22 +/- 0.29 U/g; 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide, 69.8 +/- 2.9 mmol/g; P <.05 vs ischemic control). In addition, phenylephrine (0.1 micromol/L) is protective when given before ischemia (creatine kinase, 2.06 +/- 0.21 U/g; 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide, 148.5 +/- 4.5 mmol/g; P <.05 vs ischemic control) but is detrimental when given during ischemia alone (creatine kinase, 4.49 +/- 0.98 U/g; 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide, 70.5 +/- 6.1 mmol/g; P <.05 vs ischemic control) and has no significant effect during reoxygenation. In contrast, prazosin (10 micromol/L) is beneficial when given during ischemia alone (creatine kinase, 1.34 +/- 0.10 U/g; 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide, 148.5 +/- 4.5 mmol/g; P <.05 vs ischemic control), is detrimental when given during reoxygenation alone (creatine kinase, 1.5 +/- 0.16 U/g; 3-[4,5 dimethylthiazol-2-yl]-2,5 diphenyltetrazolium bromide, 85.0 +/- 4.7 mmol/g; P <.05 vs ischemic control), and has no effect when given before ischemia. The use of phenylephrine before ischemia alone is as protective as prazosin given during ischemia alone, but the combination of the two drugs does not cause additional benefit. Interestingly, the protection afforded by phenylephrine when given before ischemia is similar to that obtained with ischemic preconditioning. CONCLUSIONS: In the human myocardium activation of alpha1-adrenoceptors before ischemia is protective but is detrimental during ischemia, whereas blockade of alpha1-adrenoceptors is beneficial during ischemia but detrimental during reoxygenation. The degree of protection achieved by activation of the alpha1-adrenoceptors before ischemia is similar to that obtained with blockade of alpha1-adrenoceptors during ischemia and that of ischemic preconditioning.

Adrenergic alpha-Antagonists↗
PubMed1994

A modified computer-assisted colorimetric microtitre assay (MTT) to assess in vitro radiosensitivity of V79, CaSki, HeLa and WiDr cells.

The non-clonogenic MTT assay, based on the reduction of a tetrazolium salt to a purple formazan precipitate by living cells, was modified and a new procedure of analysis is proposed. The colorimetric assay could be performed semi-automatically using microtitre plate reader connected to a personal computer. Data are processed and plotted with a customized program. To ensure that both control and irradiated microtitre plates contain exponentially growing cells at the time of analysis, the calculation of relative survival is based on a series of well-defined cell numbers initially seeded. To make the two endpoints of non-clonogenic and clonogenic assays comparable, i.e. counting of living cells versus counting of colonies, radiation-induced progression delay was incorporated into the calculation. Radiation-induced cell killing and progression delay could be determined in a single analysis, but in an independent way. X-ray survival curves were generated for V79, CaSki, WiDr and HeLa cells using the non-clonogenic and a standard clonogenic assay. Using the linear-quadratic formula, the resulting parameters alpha, beta and the mean inactivation dose were not significantly different. The described assay is a feasible and reproducible technique for determination of cellular survival, which may be able to incorporate progression delay. The equivalence to a clonogenic survival assay could be proven.

Animals↗
PubMed2003

Appraisal of the MTT-based assay as a useful tool for predicting drug chemosensitivity in leukemia.

The MTT-based assay relies upon the cellular reduction of tetrazolium salts to their intensely colored formazans. The test is easy to perform in hematological malignancies and is adaptable for high throughput of samples, although there are some minor limitations in its application resulting from metabolic interference. This class of assays are highly accurate for predicting drug resistance, whereas their predictive value for drug sensitivity depends on the type of disease and drug or drug combination used. They have been found to predict clinical response to fludarabine FLD in B-CLL and were useful for predetermining clinical potential of a single drug or drug combination in AML patients. Extensive studies with ALL patients have supported their advantage for selecting effective drug treatment of the disease. To conclude, pretreatment chemosensitivity assays may help in the selection of chemotherapeutic drugs with the greatest likelihood for clinical effectiveness, and in the exclusion of uneffective therapy. This can lead to improved disease management, response, survival and use of financial resources.

Antineoplastic Agents↗
PubMed2001

Application of an MTT reduction assay for assessing sperm quality and predicting fertilising ability of domestic fowl semen.

1. The ability of domestic fowl spermatozoa to reduce MTT tetrazolium to its coloured formazan was compared with other tests of sperm quality and fertilising ability. 2. MTT reduction was highly correlated with sperm ATP content (r2 = 0.85); sperm mobility (r2 = 0.62.); sperm:perivitelline layer interaction (r2 = 0.80) and fertilizing ability (r2 = 0.83). 3. The simple, robust, MTT-reduction assay may therefore be used to select male chickens on the basis of their sperm quality and thus potential fertilising ability.

Animals↗