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The respiratory chain in the cytochrome d deficient mutant Escherichia coli GR19N is a relatively simple, linear system consisting of primary dehydrogenases, ubiquinone 8, cytochrome b-556, and cytochrome o oxidase. By use of right-side-out and inside-out membrane vesicles from this strain, various oxidase activities and the generation of the H+ electrochemical gradient were studied. Oxidation of ubiquinol 1 or N,N,-N',N'-tetramethyl-p-phenylenediamine, which donate electrons directly to the terminal oxidase, generates a H+ electrochemical gradient comparable to that observed during D-lactate oxidation. In contrast, D-lactate/ubiquinone 1 or D-lactate/ferricyanide oxidoreductase activity does not appear to generate a membrane potential, suggesting that electron flow from D-lactate dehydrogenase to ubiquinone is not electrogenic. Moreover, proteoliposomes reconstituted with purified D-lactate dehydrogenase, ubiquinone 8, and purified cytochrome o catalyze D-lactate and ubiquinol 1 oxidation and generate a H+ electrochemical gradient similar to that observed in membrane vesicles. Strikingly, in inside-out vesicles, NADH oxidation generates a H+ electrochemical gradient that is very significantly greater than that produced by either D-lactate or ubiquinol 1; furthermore, NADH/ubiquinone 1 and NADH/ferricyanide oxidoreductase activities are electrogenic. It is suggested that the only component between D-lactate dehydrogenase or ubiquinol and oxygen in GR19N membranes that is directly involved in the generation of the H+ electrochemical gradient is cytochrome o, which functions as a "half-loop" (i.e., the oxidase catalyzes the scalar release of 2 H+ from ubiquinol on the outer surface of the membrane.(ABSTRACT TRUNCATED AT 250 WORDS)
The present study investigated the effect of various dietary riboflavin supplementations (0 to 4000 mg/kg) during lactation on riboflavin concentrations of liver, carcass (bled body without intestine and liver), and milk in the rat. The experiment was conducted until the 14th day of lactation; milk samples were drawn on the 7th and 13th day of lactation. Riboflavin concentrations of milk raised continuously with increasing riboflavin supplementation; in the range between 0 and 10 mg/kg riboflavin supplementation, there was a linear relationship, and in the range between 12 and 4000 mg/kg there was a logarithmic relationship between riboflavin supplementation and riboflavin concentration in the milk. Maximum riboflavin concentration of milk obtained by supplementation with 4000 mg/kg was twelve-fold higher than without riboflavin supplementation. For riboflavin supplementation up to 12 mg/kg, riboflavin concentrations in milk on the 7th day of lactation and that on the 13th day of lactation were not different. In contrast, in rats fed diets with higher riboflavin supplementation, riboflavin concentrations were higher by 25% in average in milk on the 13th day of lactation than in milk on the 7th day of lactation. Contrary to the milk, riboflavin concentrations in liver and carcass exhibited a saturation, which was achieved at a supplementation of 6 mg/kg (liver) and 10 mg/kg (carcass), respectively. Maximum riboflavin concentrations obtained at a supplementation of 4000 mg/ kg were 1.9- and 2.3-fold higher for liver and carcass, respectively, than concentrations obtained without riboflavin supplementation. The dose-response relationship using riboflavin concentrations of liver and carcass as response factors indicates a riboflavin requirement of 8 to 9 mg/kg for lactating rats fed a semisynthetic diet with 17.4 MJ ME/kg dry matter and 20.8% protein in dry matter.
Proton magnetic resonance spectroscopy (1H MRS) performed in vivo on nine Sprague Dawley rats detected a threefold increase in whole brain lactate during intravenous 1 mol/L sodium lactate infusion. Significant increases in whole brain lactate were detected within 5 min after starting lactate infusion, progressively rose to a maximum level estimated at 3.2 +/- 1.5 mmol/L (all values +/- SD) immediately postinfusion, then decreased towards baseline levels during the next hr. Venous lactate concentration, increasing from 2.3 +/- 2.4 mmol/L to 43.0 +/- 8.0 mmol/L during the infusion, exhibited a steeper rise and then decreased more rapidly in comparison to changes in whole brain lactate. These data suggest MRS can be used in vivo to study acute changes in brain lactate associated with increasing blood lactate concentrations.
Proton magnetic resonance spectroscopy (1H MRS) localized to the left temporal-parietal region in 8 healthy volunteers detected a 2.1-fold +/- 0.7-fold increase (all values +/-SD) in brain lactate during intravenous infusion of 0.5 molar (M) sodium lactate (5 meq/kg over 20 minutes). Significant increases in brain lactate occurred within 5-10 minutes after starting lactate infusion, progressively rose during the infusion, then decreased towards baseline levels during 30 minutes post-infusion. Venous lactate concentration increased from 0.8 +/- 0.2 mM to 10.9 +/- 4.1 mM or 13.6-fold during the infusion. Flow phantom findings in vitro suggest attenuation of 1H MRS blood lactate signal from arteries and veins as a result of flow velocity effects. Correlations between paired blood and brain lactate measurements at each sampling time indicate a non-linear relationship between compartments during lactate infusion.
1. The serum lipoprotein pattern was studied in four horses, four ponies and in three high producing lactating and three non-lactating cows. The lipoprotein pattern was estimated with a combination of the preparative ultracentrifugation and the heparin-manganese precipitation technique. 2. The lipid composition of the lipoproteins of horse, pony, lactating cow and non-lactating cow was determined. 3. In all three species more than 50% of serum total lipids was found in the HDL fraction. 4. The mean chylomicron fraction in horse and pony was 3.1%. In the cow it varied from 1.5 to 2.5%. 5. Between the lactating cow and the non-lactating cow there were substantial differences in the concentration of LDL and HDL. 6. The cholesterylester concentration in VLDL, LDL and HDL was clearly higher in the lactating cow than in the non-lactating cow.
The ecotoxicity of lactic acid, its alkyl esters and selected metal salts was studied experimentally with the micro alga Selenastrum capricornutum, the crustacean Daphnia magna and the fish species Brachydanio rerio and Pimephales promelas. In addition, the biodegradation of lactate esters was also studied. The aim of the study was to provide predicted environmental data for additional alkyl homologues and metal salts. The ecotoxicity data are evaluated by means of Structure Activity Relations (SAR), using literature data on a non-polar narcotic mechanism of toxicity as a baseline for comparison. Lactate salts were evaluated by comparison to the toxicity of the metal ion. For the fish and D. magna, it was evident that methyl, ethyl, propyl and to a lesser extent butyl lactate were slightly more toxic in comparison to baseline non-polar narcotic toxicity data. The toxicity tests carried out with lactate-salts demonstrated clearly that the toxicity in standard tests is only determined by the associated cation and not by the lactate part. Lactic acid and its alkyl esters were degraded for more than 60% in the ready biodegradability tests and from the data presented, it is evident that the majority of alkyl lactates are readily biodegradable. The results presented in this study indicate that alkyl lactate esters show some differences in their ecotoxicity when compared to non polar narcotic compounds in but that these differences are generally small. When aquatic toxicity is considered together with their rapid tendency to biodegrade, it is concluded that lactate esters show generally favourable environmental characteristics.
This study summarizes weight development, plasma glucose concentrations and reproductive parameters in lactating (n = 46) and non-lactating Lipizzaner mares (n = 11) throughout the breeding season. It was the aim of the study to analyse if an energy deficit with possible effects on reproductive functions occurs at any time during the first 4 months of gestation. Mean gestation length was 334.3 +/- 7.3 days. Gestation of foals born in May/June was shorter (P < 0.01) than for foals born in March/April. Out of the 46 lactating mares, 44 ovulated between Days 8 and 18 postpartum and two mares ovulated on days 30 and 145, respectively. Pregnant mares were significantly (P < 0.001) heavier (600.1 +/- 5.3 kg) than non-pregnant mares (521.8 +/- 10.0 kg) at the beginning of the study. Birth resulted in weight reduction of 64.8 +/- 2.4 kg. During the first 2 weeks postpartum mares lost on average 3.0 +/- 1.8 kg and in the following 2 weeks gained 3.6 +/- 1.4 kg of weight. Thereafter, weight increased slightly but continuously (P < 0.01). At no time after foaling, weight differed significantly between groups. Weight of the foals three days after birth varied between 29 and 67 kg (53.7 +/- 1.1 kg). Average daily weight gain of foals was relatively constant throughout the study period (1.15 +/- 0.17 kg). Although lactation at no time was associated with a major weight loss, it had clear effects on energy metabolism as shown by constantly lower plasma glucose concentrations in lactating mares. Glucose concentrations decreased after foaling and were significantly lower in lactating mares from Weeks 3 to 16 after foaling than at corresponding times in non-lactating mares (P < 0.01). However, glucose concentrations were still within the physiological range. Mares seem to be able to compensate energy losses during lactation mainly by increasing feed intake and not by mobilisation of body fat.
We conducted an experiment in dairy cows investigating the effects of calving season, milking frequency and nutrition on lactation persistency. Cows calved in the Spring (n=12) or Winter (n=12). Commencing in lactation week 9 one udder-half of each cow was milked thrice-daily and half of each calving group received additional concentrate at a fixed rate of 3kg per day above that of the control cows. As reported elsewhere, between lactation weeks 9 and 33 persistency (measured as the slope of decline in milk yield) was significantly improved by frequent milking (P<0.001), by calving in the Winter (P<0.001) and by additional concentrate (P<0.05). The cows were rebred after week 33. When analysis of persistency was extended up to week 20 of the recurring pregnancy only the frequency effect remained significant. Persistency was unaffected by the pregnancy up until pregnancy week 20 but was then greatly reduced (P<0.001). In this paper we report hormone concentrations. GH was unaffected by nutrition but was consistently elevated in the Winter calving group relative to the Spring. IGF1 and prolactin were both unaffected by nutrition and calving season, IGF1 tended to increase as lactation progressed but changes in prolactin were related to time of year more than stage of lactation. Insulin was not affected by nutrition and was lower in Winter calvers, but only during early lactation. Prior to rebreeding, lactation persistency was correlated (slightly) with [GH] but not with [IGF1] or [insulin] and was correlated significantly with changes in GH, IGF1 (both positive) and insulin (negative). In conclusion, whilst bovine lactation persistency is plastic and amenable to beneficial manipulation, the details of its endocrine control remain to be elucidated.
We measured daily energy expenditure (DEE) and water turnover rates in lactating and non-lactating short beaked echidnas (Tachyglossus aculeatus) using the doubly labelled water technique during the lactation period in spring. Reproductively inactive echidnas were on average significantly heavier (median: 3354 g; range: 2929-3780 g; N=4) than lactating females (median: 2695 g; range: 2690-2715 g; N=3) during the equivalent time period. The median water flux rate of lactating echidnas (152 ml day(-1); range: 120-198 ml day(-1)) did not differ significantly from that of non-lactating females (170 ml day(-1); range: 128-227 ml day(-1)). The median DEE of echidnas that were lactating was 645 kJ day(-1) (range: 581-850 kJ day(-1)), which was not different from the median DEE of non-reproductive control females (763 kJ day(-1); range: 720-766 kJ day(-1)). Lactating females somehow compensate for the energy costs of milk production, resulting in a daily energy budget that is not different from that of non-reproductive females. At least part of their energy minimising strategy could involve the use of moderate heterothermy, allowing a greater proportion of daily energy expenditure to diverted to milk production.
Changes in production parameters and metabolite biokinetics induced by treatment with pituitary-derived bovine growth hormone (bGH) were monitored at peak (c. 40 days) and mid-lactation (c. 130 days) in dairy cows. During treatment with bGH milk production increased by 6 and 14% at peak and mid-lactation respectively. At peak lactation the content of milk fat tended to increase, whereas milk protein tended to decrease and milk lactose decreased significantly. Yield of milk fat increased, but there was no change in the yield of milk protein and lactose. The content of milk fat tended to increase at mid-lactation. Milk protein decreased and there was no change in milk lactose. Yields of milk fat and lactose but not protein increased. Growth hormone exerted metabolic effects which differed with stage of lactation. At peak lactation plasma glucose concentration and its irreversible loss increased, plasma urea and acetate were unchanged and their irreversible losses tended to increase. No change was measured for plasma non-esterified fatty acids (NEFA) and the irreversible loss of NEFA decreased. At mid-lactation plasma concentrations of glucose and NEFA were increased, plasma urea decreased and acetate and 3-hydroxybutyrate tended to increase. Irreversible losses of NEFA increased, urea tended to decrease and acetate and glucose remained essentially constant. The results show that exogenous pituitary bGH exerts metabolic effects which result in the supply of increased nutrients to support milk synthesis. The metabolic effects differ with the stage of lactation, reflecting differences in physiological and/or nutritional state.
We have investigated the effects of maternal vitamin A intake during pregnancy and lactation or during lactation alone on the concentration of vitamin A in rat's milk and on vitamin A levels in plasma and liver of dams and their pups. Groups of Sprague-Dawley rats were fed diets having either a high vitamin A content [15 retinol equivalents (R.E.)/g diet] or a low vitamin A content (0.6 R.E./g) for 42 d, including 7-8 d prior to pregnancy, pregnancy, and for 14 d of lactation. The concentration of vitamin A in milk on d 14 of lactation was significantly greater on the high vitamin A diets [114 +/- 16 micrograms/dl (mean +/- SEM; n = 8) versus 52 +/- 7.3 micrograms/dl (n = 11), P less than 0.005]. However, milk vitamin A concentration on d 1 of lactation did not vary with maternal vitamin A intake during pregnancy. In a second study in which supplementation with vitamin A (30 R.E./g diet) was begun on d 1 postpartum, the milk vitamin A content increased progressively with duration of lactation. Maternal plasma vitamin A concentrations did not differ between rats fed the higher or lower vitamin A diets. However, liver vitamin A concentrations both of dams and of their 14-d-old pups were significantly higher when dams were fed the higher vitamin A diets during pregnancy and/or lactation. The results of these studies indicate that the transfer of vitamin A from mother to offspring by milk and the vitamin A status of dams and their suckling neonates is influenced by maternal vitamin A intake during lactation.(ABSTRACT TRUNCATED AT 250 WORDS)