Maternal perinatal transfer of vitamins and trace elements to piglets

Nursing piglets are entirely dependent, for their micronutrient provisions, upon in utero, colostrum and milk transfers from the dam. An adequate maternal transfer of micronutrients is all the more important during these periods which, in fact, lasts for approximately half the life cycle (conception to slaughter) of modern pigs. The present study aimed to set up a simple approach to assess the maternal perinatal transfer of vitamins and trace elements in sows. Prenatal transfer (R-u) was estimated as limited, passive or active using the ratio between pre-colostral serum concentrations of a given micronutrient in newborn piglets and corresponding pre-farrowing values in sows. Efficiency of the postnatal transfer (R-c) was estimated from the ratio between serum concentrations of post- and pre-colostral micronutrients in piglets. Data from literature (12 studies) were used for vitamins A, D, E, C, folic acid and B₁₂, whereas vitamins B₂, B₃, B₆ and B₈ as well as Zn, Fe, Cu and Se were generated from a trial where blood sera from 20 sows, and their litter were collected during the perinatal period. In sow trial, statistical t tests were used to determine if ratios differed from 1. Prenatal transfer was active and in favour of piglets (R-u > 1, P < 0.03) for Zn and vitamins B₆ and B₈ (sow trial) as well as for vitamins C and B₁₂ (literature data). This transfer was limited (R-u < 1, P < 0.01) for vitamin B₂, Fe, Cu and Se (sow trial) and for vitamins A, E, D and folic acid (literature data) whereas it was passive for vitamin B₃ (R-u = 1, P > 0.37). After birth, the early postnatal transfer through colostrum was active towards piglets for most micronutrients but vitamins B₆ and B₈ (R-c < 1, P < 0.01). Globally, the perinatal transfer (combination of R-u and R-c) was favourable to the neonatal piglets for most micronutrients except for vitamins A and D as well as Fe, Cu and Se whereas there is apparently a barrier for prenatal transfer which is not compensated by the colostrum provision to neonatal piglets. Then, post-colostral concentrations of these micronutrients in piglets remain below prenatal levels of their dam. Neonatal strategies of micronutrient provision are known for Fe (intramuscular injection) and Se (sow milk enrichment). Further studies are needed to assess the importance of the unfavourable perinatal transfer for Cu and vitamins A and D for piglet robustness later in life.     

Maternal hypoxia increases the activity of MMPs and decreases the expression of TIMPs in the brain of neonatal rats

A recent study has shown that increased activity of matrix metalloproteinases‐2 and metalloproteinases‐9 (MMP‐2 and MMP‐9) has detrimental effect on the brain after neonatal hypoxia. The present study determined the effect of maternal hypoxia on neuronal survivability and the activity of MMP‐2 and MMP‐9, as well as the expression of tissue inhibitors of metalloproteinase 1 and 2 (TIMP‐1 and TIMP‐2) in the brain of neonatal rats. Pregnant rats were exposed to 10.5% oxygen for 6 days from the gestation day 15 to day 21. Pups were sacrificed at day 0, 4, 7, 14, and 21 after birth. Body weight and brain weight of the pups were measured at each time point. The activity of MMP‐2 and MMP‐9 and the protein abundance of TIMP‐1 and TIMP‐2 were determined by zymography and Western blotting, respectively. The tissue distribution of MMPs was examined by immunofluorescence staining. The neuronal death was detected by Nissl staining. Maternal hypoxia caused significant decreases in body and brain size, increased activity of MMP‐2 at day 0, and increased MMP‐9 at day 0 and 4. The increased activity of the MMPs was accompanied by an overall tendency towards a reduced expression of TIMPs at all ages with the significance observed for TIMPs at day 0, 4, and 7. Immunofluorescence analysis showed an increased expression of MMP‐2, MMP‐9 in the hippocampus at day 0 and 4. Nissl staining revealed significant cell death in the hippocampus at day 0, 4, and 7. Functional tests showed worse neurobehavioral outcomes in the hypoxic animals. © 2009 Wiley Periodicals, Inc. Develop Neurobiol 2010     

Peculiarities of proteasome pool formation in rat spleen and liver during postnatal development

Changes in the specific activity and amounts of 26S and 20S proteasome pools in rat spleen and liver during postnatal development and appearance in them of immune subunits were studied. Two decreases in chymotrypsin-like activity of the proteasome pools were recorded during the first three weeks after birth. The activity minimum fell on the 11th and 19th days, and the first decrease was more prolonged and pronounced than the second. The decrease in the specific activity of the 26S proteasome pools was associated with a reduction of their quantity. The 20S proteasome pools displayed no such decreases. Noticeable quantities of immune subunits LMP7 and LMP2 were revealed by Western blotting in the spleen on the 7th day and on the 19th day in the liver, concurrently with the beginning of the decrease in the proteasome activity. It was concluded that during the first three weeks of postnatal development the proteasome pools in rat spleen and liver were replaced twice, and in the spleen (a lymphoid organ) a qualitatively new pool containing immune subunits appeared nearly two weeks earlier than in the liver (a non-lymphoid organ). The appearance of immune proteasomes in different organs and tissues during some weeks after birth seems to explain the immune system inefficiency during embryogenesis and early postnatal development.     

Postnatal developmental expression and localization of apelin and apelin receptor protein in the ovary and uterus of mice

Postnatal ovarian and uterine development is crucial to accomplished female fertility. Thus, the investigations of factors that present in pre-pubertal stages are important as it might be responsible for the regulation of ovarian and uterine function. Apelin, an adipokine and its receptor (APJ) are present in female reproductive organs. However, no study has reported its postnatal expression in uterus and ovary. Thus, we investigated the postnatal developmental changes in expression and localization of apelin and APJ in the ovary and uterus of mice. Postnatal ovary and uterus were collected from postnatal day (PND) 1, 7, 14, 21, 42, 65 and performed western blot analysis and immunohistochemistry. Uterine APJ is elevated in PND14 and PND65, whereas, ovarian APJ elevated in PND7, PND14, and PND65. Apelin expression in both ovary and uterus showed intense staining at PND65 and PND14. Our results showed that apelin and APJ abundance was lower at PND21 in uterus and ovary. In conclusion, apelin and APJ are developmentally regulated in the ovary and uterus, and its localization in the different compartments of ovary and uterus suggest its distribution specific physiological role in the uterus and ovary.     

Maternal nutrition and the programming of obesity

The increasing incidence of obesity in the developed and developing world in the last decade has led to a need to define our understanding of the physiological mechanisms which can predispose individuals to weight gain in infancy, childhood and adulthood. There is now a considerable body of evidence which has shown that the pathway to obesity may begin very early in life, and that exposure to an inappropriate level of nutrition during prenatal and/or early postnatal development can predispose individuals to obesity in later life The brain is at the heart of the regulation of appetite and food preferences, and it is increasingly being recognised that the development of central appetitive structures is acutely sensitive to the nutritional environment both before and immediately after birth. This review will summarise the body of work which has highlighted the critical role of the brain in the early origins of obesity and presents some perspectives as to the potential application of these research findings in the clinical setting.     

Reproductive biology and postnatal development in the tent-making bat Artibeus watsoni (Chiroptera: Phyllostomidae)

In this study we investigated the reproductive patterns and postnatal development in the tent-making bat Artibeus watsoni . We sampled two populations in the Golfito Wildlife Refuge and Corcovado National Park, south-western Costa Rica, from June 2003 to March 2005. Most females were pregnant during the months of January and June, and most were lactating in March and July, indicating that this species exhibits seasonal bimodal polyoestry, with the first parturition peak occurring in February–March and the second in June–July. Additionally, we observed a postpartum oestrus following the first parturition, but not after the second. Females entered oestrus again in November–December and had a gestation period of c . 3 months. A female-biased sex ratio of neonates was observed during the second parturition period, and young were born at 32 and 56% of their mothers' body mass and length of forearm, respectively. Adult proportions in length of forearm were attained faster than adult proportions in body mass, and sustained flight was only possible after 35 days of age, when pups had achieved 100 and 80% of adult length of forearm and body mass proportions, respectively. Weaning and roosting independence occurred when young were c . 30–40 days old, and young females appeared to remain close to their place of birth, at least for their first mating period, whereas adult males were never recaptured near their birth site. In addition, sexual maturity was reached in as little as 3 months in females born during the first parturition period, whereas females born during the second birth period in June–July seemed to reach maturity at 6 months of age. Our results show that A. watsoni belongs to the faster lane of the slow–fast continuum of life-history variation in bats, which may be attributed primarily to its roosting and feeding ecology.     

Maternal nutritional programming of fetal adipose tissue development: long-term consequences for later obesity

As obesity reaches epidemic levels in the United States there is an urgent need to understand the developmental pathways leading to this condition. Obesity increases the risk of hypertension and diabetes, symptoms of which are being seen with increased incidence in children. Adipocyte development begins in the fetus and, in contrast to all other tissues whose growth ceases in late juvenile life, it has the capacity for "unlimited" growth. In normal healthy individuals, the increase in fat mass with age is accompanied by a parallel increase in cortisol sensitivity, i.e., increased glucocorticoid receptor abundance and increased activity of the enzyme 11beta hydroxysteroid dehydrogenase type 1. Enhanced adipocyte sensitivity to cortisol is promoted in offspring born to mothers that were nutrient-restricted in utero in conjunction with increased peroxisome proliferator activated receptor alpha. This adaptation only appears to be associated with greater fat mass in the offspring when maternal nutrient restriction is confined to late gestation, coincident with the period of maximal fetal growth. In these offspring, increased fat mass is accompanied by glucose intolerance and insulin resistance, in conjunction with an adipose tissue specific reduction in glucose transporter 4 abundance. In conclusion, changes in maternal and, therefore, fetal nutrient supply at specific stages of gestation have the potential to substantially increase the risk of those offspring becoming obese in later life. The extent to which changes in dietary habits, both during pregnancy and in later life, may act to contribute to the current explosion in childhood and adult obesity remains a scientific and public health challenge to us all.     

Postnatal development of phospholipids and their fatty acid profile in rat heart

The aim of this study was to determine the concentration of phospholipids (PL), plasmalogen components of choline (PC) and ethanolamine (PE) phosphoglycerides (PLPC, PLPE) and fatty acid profile of PL and triacylglycerols (TAG) in developing rat left ventricular myocardium between postnatal day (d) 2 and 100. The steepest increase of total PL (TPL) concentration occurs between d2 and d5, followed by a further slower increase between d20 and d40. Similar developmental changes were observed in PC and PE. The PLPE concentration rises by d10, whereas PLPC does not change during the whole period investigated, except for the transient decline on d5. The concentration of diphosphatidylglycerol (DPG) increases by d60; the steepest rise occurs between d20 and d40. Phosphatidylinositol (PI) concentration rises only by d5. The concentration of phosphatidylserine (PS) decreases between d5 and d10 and then it does not change. Sphingomyelin (SM) concentration is maintained till d10, it declines on d20 and does not change thereafter. The proportion of saturated fatty acids (SFA) increases by d5 in PC, PE, PS and TAG, and by d10 in DPG and PI. After d20 the SFA proportion gradually decline in all lipids. Monounsaturated FA (MUFA) proportion decreases in PC, PE, PI and PS from d2 till d10, and in the weaning period it tends to rise again. In contrast, in DPG and TAG the proportion of MUFA declines during the whole postnatal period. N-6 polyunsaturated FA (PUFA) decrease in all PL by d20 and rise again thereafter; in TAG they decline between d2 and d10 and return to the initial level by d100. N-3 PUFA increase in all PL during the suckling period and decline after weaning; in TAG they increase only by d5 and then they decline. This remodeling of myocardial PL and TAG composition during postnatal development may affect membrane properties and contribute to developmental changes in the function of membrane proteins and cell signaling.     

Review: passive immunity in beef-suckler calves

Colostrum-derived passive immunity is central to the health, performance and welfare of neonatal beef-suckler calves, and economics of beef-farming enterprises. Compared to dairy calves, mainly Holstein-Friesian, there is much less research carried out on passive immunity and associated factors in beef calves. Thus, this review aimed to summarise and interpret published information and highlight areas requiring further research. The transfer of immunoglobulin G1 (IgG1) from blood to mammary secretions is greater for beef × dairy cows compared to most beef breed types. Considerable between-animal variance is evident in first-milking colostrum yield and immunoglobulin concentration of beef-suckler cow breed types. First-milking colostrum immunoglobulin concentrations are similar for within-quarter fractions and for the front and rear quarters of the udder. First-milking colostrum yield is higher for beef × dairy cows than beef × beef and purebred beef breeds, and higher for multiparous than primiparous cows, but generally colostrum immunoglobulin concentration is relatively similar for each of the respective categories. Consequently, colostrum immunoglobulin mass (volume × concentration) production in beef cows seems to be primarily limited by colostrum volume. The effect of maternal nutrition during late gestation on colostrum yield is not well documented; however, most studies provide evidence that colostrum immunoglobulin concentration is not adversely affected by under-nutrition. Factors that impinge upon the duration between birth and first suckling, including dam parity, udder and teat anatomy and especially dystocia, negatively impact on calf passive immunity. Colostrum immunoglobulin mass ingested relative to birth weight post-parturition is the most important variable determining calf passive immunity. Research indicates that feeding the beef calf a colostrum volume equivalent to 5% of birth weight shortly after parturition, with subsequent suckling of the dam (or a second feed) 6 to 8 h later, ensures adequate passive immunity, equivalent to a well-managed suckling situation. Within beef-suckler cow genotypes, calf passive immunity is similar for many common beef breeds, but is generally higher for calves from beef × dairy cows. Compared to older cows, calves from younger cows, especially primiparous animals, have lower serum immunoglobulin concentrations. Most studies have shown no adverse impact of maternal dietary restriction on calf passive immunity. The prevalence of failure of passive transfer (FPT) in beef calves varies considerably across studies depending on the test used, and what cut-off value is assumed or how it is classified. The accuracy and precision of methodologies used to determine immunoglobulin concentrations is concerning; caution is required in interpreting laboratory results regarding defining colostrum ‘quality’ and calf passive immune ‘status’. Further research is warranted on colostrum-related factors limiting passive immunity of beef calves, and on the validation of laboratory test cut-off points for determining FPT, based on their relationships with key health and performance measures.     

Postnatal development of rat pups after maternal exposure to diethanolamine

BACKGROUND: Diethanolamine (DEA), a widely used surfactant, was administered to pregnant mice at the oral LD10 resulting in failure of pups to grow and thrive through postnatal day (PND) 3 [National Toxicology Program, 1987; York et al., Teratology 37:503-504, 1988]. The toxicity profile for DEA differs among rodent species. This study investigated DEA-induced postnatal toxicity in a second species. METHODS: Timed-mated Sprague-Dawley rats were dosed (0, 50, 125, 200, 250, or 300 mg DEA/kg/day, p.o.) on gestational days (GD) 6-19. Dams and pups were monitored for body weight, feed/water intake, clinical signs, litter size, and sex ratio. At necropsy (PND 21), maternal liver and kidney weights and number of uterine implantation sites were recorded. RESULTS: The high-dose group was terminated early due to excessive toxicity. The estimated maternal LD10 was 218 mg/kg/day. Maternal effects included decreased body weight and relative feed intake (>or=200 mg/kg/day), transiently reduced relative water intake (125 and 250 mg/kg/day), and increased absolute kidney weight (>or=125 mg/kg/day). Postimplantation loss (PND 0) and pup mortality (PND 0-4) were increased (>or=200 and >or=125 mg/kg/day, respectively). Pup body weight was reduced (>or=200 mg/kg/day) as late as PND 21. CONCLUSIONS: This study demonstrates reduced postnatal growth and survival in a second species after gestational exposure to DEA, persistence of toxic effects through the end of lactation, possibly due to long elimination half-life, and maternal and developmental toxicity no-observed-adverse-effect level (NOAELs) (50 mg/kg/day) and lowest-observed-adverse-effect level (LOAELs) (125 mg/kg/day) for oral DEA exposure during embryo/fetal development in the rat.     

Pre- and postnatal development studies of lasofoxifene, a selective estrogen receptor modulator (SERM), in Sprague-Dawley rats

BACKGROUND: Lasofoxifene is a nonsteroidal selective estrogen receptor modulator (SERM) developed for the treatment of postmenopausal osteoporosis. The purpose of these studies was to evaluate the effects of lasofoxifene on the postnatal development, behavior, and reproductive performance of offspring of female rats given lasofoxifene during organogenesis and lactation. METHODS: Two range-finding studies were conducted to determine the effects of lasofoxifene at doses from 0.01-10 mg/kg on parturition and lactation in pregnant rats and on the early postnatal development of the offspring, and to optimize the dosing regimen. Maternal milk and plasma were sampled for concentrations of lasofoxifene on Lactation Days 4, 7, and 14. In the pre- and postnatal development study, lasofoxifene was administered to pregnant and lactating rats by oral gavage at dose levels of 0.01, 0.03, and 0.1 mg/kg on Gestation Days 6-17 and Lactation Days 1-20. Maternal body weight and food consumption were measured throughout pregnancy, and body weight was measured throughout lactation. Parturition was monitored closely. The F1 offspring were measured for viability, body weight, anogenital distance, the appearance of postnatal developmental indices and reflex behaviors, sensory function, in an age-appropriate functional observational battery, motor activity, auditory startle, passive avoidance, and the Cincinnati Water Maze. The F1 generation was assessed for reproductive function, and the F2 offspring were measured for body weight and viability throughout the lactation period. RESULTS: In the range-finding studies, indications of maternal toxicity included decreased body weight and food consumption, increased length of gestation, prolonged parturition, dystocia, and increased offspring mortality at birth. Concentrations of lasofoxifene in maternal plasma were similar to those in milk, increased with increasing dose, and remained consistent over a 10-day period. In the pre- and postnatal development study, maternal body weights and food consumption were decreased in all treated groups during gestation. Length of gestation was increased, parturition was prolonged, and dystocia was noted in the dams in the 0.1 mg/kg group. There was increased pup mortality in the F1 litters in the 0.1 mg/kg group and all treated groups had decreased offspring body weights beginning at 1 week of age, continuing into the postweaning period and, for the F1 males, into adulthood. Female F1 offspring in the 0.03 and 0.1 mg/kg groups had increased body weights as adults. There were delays in the age of appearance of preputial separation in the males in the 0.1 mg/kg group and vaginal opening in the females in all treated groups. Body temperature was decreased by <0.5 degrees C after weaning for male and female offspring in the 0.1 mg/kg group. The sensory, behavioral, and functional measures, including the tests of learning and memory, were unaffected by treatment. Mating success was lower for the F1 animals in the 0.1 mg/kg group, but there were no effects on the reproductive parameters. Mating, reproduction, and maternal behavior of the F1 animals in the 0.01 and 0.03 mg/kg groups and the survival and body weights of the F2 offspring in all treated groups through Postnatal Day 21 were unaffected by treatment. CONCLUSION: The maternal findings in this study were related to the pharmacologic activity of lasofoxifene. Inhibition of growth of the F1 offspring after perinatal exposure to lasofoxifene was observed, but there were no significant effects on the sensory, behavioral, or functional measures, including learning and memory. There were no effects on the F2 generation. The findings are consistent with those reported for at least one other SERM. The findings of this study do not suggest increased risk for the primary indication of use in postmenopausal women.     

Review: kisspeptin and reproduction in the pig

The activation of the hypothalamic–pituitary axis is critical for the initiation and maintenance of reproductive cycles in pigs and is influenced by a number of factors, such as nutrition, metabolism and gonadal steroids. Kisspeptin is a neuropeptide that is expressed in discrete regions of the porcine hypothalamus and is positioned to mediate the action of many of these factors. The expression of kisspeptin in the pig hypothalamus does not appear to be regulated by gonadal steroids in the same way as other species. It is unclear if kisspeptin is mediating nutritional or metabolic effects on gonadotropin secretion in pigs as it takes large deficits in feed intake or BW to affect hypothalamic expression of the KISS1 gene in the porcine hypothalamus. There appears to be little genetic diversity in kisspeptin or its receptor that is useful for improving reproduction in swine. Both peripheral and central injection of kisspeptin strongly stimulates the secretion of gonadotropin hormones, LH and FSH, in gilts. Similarly, synthetic analogues have been developed and showed potential promise as tools to manage reproductive cycles in gilts and sows. Review of the literature nonetheless reveals that research on kisspeptin and its function in controlling reproduction in pigs has lagged that of other livestock species.     

Expression of low-molecular-weight neurofilament (NF-L) mRNA during postnatal development of the mouse brain

A regional Northern blot analysis demonstrated that the highest levels of NF-L mRNA in the adult mouse brain are present in brain stem followed by mid-brain, with lower levels found in neocortex, cerebellum, and hippocampus. The study was extended to the cellular level over the time course of postnatal development using in situ hybridization. This developmental analysis revealed that the expression of NF-L mRNA closely follows the differentiation pattern of many large neurons during postnatal neurogenesis. Neurons which differentiate early such as Purkinje, mitral, pyramidal, and large neurons of brain stem and thalamic nuclei, expressed high levels of NF-L mRNA at postnatal day 1. Early expression of NF-L mRNA may be required for the maintenance of the extensive neurofilament protein networks that are detected within the axons of larger neurons. Smaller neurons which differentiate later, such as dentate gyrus granule cells, small pyramidal and granule cells of the neocortex, and granule cells of the cerebellum, exhibit a delayed expression of NF-L mRNA.To whom to address reprint requests.     

Regulation of fetuin A gene expression in the neonatal pig liver

Fetuin A (also known as α2-Heremans–Schmid glycoprotein) is a protein primarily expressed by the liver and secreted into the blood. Previous studies have suggested that plasma concentrations of fetuin A are elevated with impaired growth rate in swine. The present study was designed to examine the relationship of porcine fetuin A with growth rate in the pig and to also elucidate the regulation of fetuin A expression by examining the hormonal and cytokine regulation of fetuin A mRNA abundance in hepatocytes prepared from suckling piglets. Quantitative real-time PCR assay was used to quantify the number of fetuin A mRNA molecules/molecule cyclophilin mRNA. Total RNA was isolated from liver of three different groups of pigs to assess changes in mRNA abundance of fetuin A: normal piglets at day 1, day 7 day 21 or 6 months of age (n=6 for each age); runt and control piglets at day 1 of age (n=4); slow growing and normal growing piglets at 21 days of age (n=8). Following birth, fetuin A gene expression increased from day 1 and 7 of age (P<0.05), and then declined at 21 days of age (P<0.05), with a much greater decline to 6 months of age (P<0.01). Fetuin A mRNA abundance was higher in runt pigs v. their normal birth weight littermates (P<0.05). Similarly, fetuin A gene expression was higher in livers of pigs that were born at a normal weight but that grew much slower than littermates with the same birth weight (P<0.05). Hepatocytes were isolated from preweaned piglets and maintained in serum-free monolayer culture for up to 72 h to permit examination of the influences of hormones, cytokines and redox modifiers on fetuin A mRNA abundance. Fetuin A gene expression was enhanced by glucagon, T3 and resveratrol (P<0.05). Growth hormone, cytokines (interleukin6, tumor necrosis factor-α) and antioxidants (N-acetylcysteine, quercertin) reduced fetuin A mRNA abundance (P<0.05). A role for fetuin A in postnatal development is suggested by the differences in fetuin A mRNA abundance between runt piglets or slow growing piglets and their normal growing sized littermates. The hepatocyte experiments suggest multiple hormones and cytokines may contribute to the regulation of fetuin A during early growth of the pig.     

A mathematical model of epiphyseal development: hypothesis on the cartilage canals growth

The role of cartilage canals is to transport nutrients and biological factors that cause the appearance of the secondary ossification centre (SOC). The SOC appears in the centre of the epiphysis of long bones. The canal development is a complex interaction between mechanical and biological factors that guide its expansion into the centre of the epiphysis. This article introduces the ‘Hypothesis on the growth of cartilage canals’. Here, we have considered that the development of these canals is an essential event for the appearance of SOC. Moreover, it is also considered to be important for the transport of molecular factors (RUNX2 and MMP9) at the ends of such canals. Once the canals are merged in the centre of the epiphysis, these factors are released causing hypertrophy of adjacent cells. This RUNX2 and MMP9 release occurs due to the action of mechanical loads that supports the epiphysis. In order to test this hypothesis, we use a hybrid approach using the finite element method to simulate the mechanical stresses present in the epiphysis and the cellular automata to simulate the expansion of the canals and the hypertrophy factors pathway. By using this hybrid approach, we have obtained as a result the spatial–temporal patterns for the growth of cartilage canals and hypertrophy factors within the epiphysis. The model is in qualitative agreement with experimental results previously reported by other authors. Thus, we conclude that this model may be used as a methodological basis to present a complete mathematical model of the processes involved in epiphyseal development.     

Additional studies of sheep haemopexin: genetic control,frequencies and postnatal development*

Summary. This study presents evidence that sheep haemopexin phenotypes are genetically controlled by three alleles, Hpx^A, Hpx^B1 and Hpx^B2, of a single autosomal locus. Frequencies of two alleles, Hpx^A and Hpx^B (Hpx^B encompasses two isoalleles, Hpx^B1 and Hpx^B2), were studied in eight sheep breeds in Czechoslovakia. The frequency of the HpxA allele was highest (ranging from 0.81 in Merino to 1.0 in East Friesian sheep). Qualitative and quantitative changes in haemopexin during postnatal development were studied by starch gel electrophoresis and rocket immunoelectrophoresis respectively. In electrophoresis, 1- or 2-day-old lambs had two very weak zones corresponding in mobility to two slower zones of adult animals. Later, the third more anodic zone appeared and gradually increased in intensity. In 1-month-old lambs the patterns were practically identical with those of adult animals. Using rocket immunoelectrophoresis, the level of haemopexin shortly after birth was practically zero. It rose sharply till the sixth day of life; then the level continued to rise slowly till about 1 month of age. The mean haemopexin level in adult sheep was 64.5 ± 18.26 (SD) mg/100ml serum, ranging from 30.5 to 116.5 mg/100ml.