Two domestic guinea-pigs (Cavia porcellus), bought in Pinheiros, São Paulo State, Brazil, were taken by their owners a farm in the rural district of Capão Bonito, close to the Atlantic Forest, São Paulo, where they both developed tumour-like and ulcerating lesions on the ears. The causative agent was identified as Leishmania (L.) enriettii, based on biological characters and isoenzyme profiles. Sources of the parasite in wild mammals, and the possible sandfly vector species discussed.

Mild-to-moderate vitamin C depletion in weanling guinea-pigs affects pyridinoline:deoxypyridinoline (collagen cross-link) ratios in femur shaft and urine, attributed to impairment of hydroxylation of collagen lysine. We investigated: (1) whether the picture at two time points is compatible with progressive accumulation of abnormal collagen; (2) whether any changes are seen in skin, where little deoxypyridinoline occurs; (3) whether total food restriction has similar effects. Male weanling Dunkin–Hartley guinea-pigs were fed diets containing either 0·5 (vitamin C-restricted) or 160·0–320·0 (vitamin C-adequate) mg vitamin /. Two groups receiving the vitamin C-adequate diet received it ad libitum. Two other groups received the vitamin C-adequate diet in a restricted amount, limited to that which permitted nearly the same growth rate as in the vitamin C-restricted groups. Animals were fed for 4 or 8 weeks; urine was collected, and vitamin C and collagen indices were measured. In the femur shaft, the hydroxyproline content per unit weight was unaffected by vitamin C restriction or by total food restriction. Deoxypyridinoline was increased and the pyridinoline:deoxypyridinoline ratio was decreased in vitamin C-restricted groups, but not in food-restricted groups. Changes in the value of the ratio were greater after 8 than after 4 weeks. Urine indices mirrored bone indices. In skin, the main effect of vitamin C restriction was to reduce hydroxyproline. Here, the cross-link ratios changed less markedly than in bone, and there was less deoxypyridinoline. We conclude that the picture at two time points is compatible with a progressive accumulation of pyridinoline-enriched collagen in vitamin C-deprived animals, that the picture in skin differs from that of bone and urine, and that cross-link changes are not produced by total food restriction.

Guinea-pig fetuses at term are mineralized to a degree comparable with human fetuses, which makes the guinea-pig an attractive animal model to study maternal–fetal interactions with regard to Ca and phosphate (P) homeostasis. We studied non-pregnant and pregnant (day 57) vitamin D-replete guinea-pigs, fed either a normal guinea-pig chow with 9·6 g Ca/kg and 4·9 g P/kg or a study diet with 2 g Ca/kg and 1 g P/kg (low-Ca–P diet) for 7–8 weeks. Both pregnancy and the low-Ca–P diet decreased plasma concentrations of 25-hydroxycholecalciferol (25(OH)D3), but increased total and free 1α,25-dihydroxycholecalciferol (1,25(OH)2D3), strongly suggesting an additive stimulation of 1α-hydroxylase activity. Maternal and fetal 25(OH)D3 and 1,25(OH)2D3 levels were highly correlated (r 0·82 and 0·92 respectively, P<0·001). Dual-energy absorption X-ray absorptiometry (DXA) showed that both pregnancy and the low-Ca–P diet decreased bone mineral density (BMD) of the maternal femur, particularly at the distal metaphysis. Despite higher 1,25(OH)2D3 concentrations and lower BMD, pregnant animals on the low-Ca–P diet were hypocalcaemic; blood Ca2+ levels were inversely correlated with the number of fetuses in this group (r -0·93, P<0·001). Fetal growth as well as mineralization (assessed by whole-body and femoral DXA, bone histomorphometry and plasma–bone osteocalcin measurements) were unaltered in the low-Ca–P group. In conclusion, fetal mineralization proceeds normally but induces maternal hypocalcaemia in guinea-pigs with dietary restriction of Ca and P.

The effects of maternal intake and gestational age on materno-fetal transport of vitamin C were investigated in female Dunkin-Hartley guinea-pigs. Twenty-four time-mated dams were fed on either a moderate-vitamin C (group A) or a high-vitamin C (group B) diet, throughout pregnancy. At days 49, 63 and 66 of gestation, and at term, three animals from each group were killed and fetuses removed by hysterectomy. Plasma, liver, kidney, lungs, heart, placenta and amniotic fluid were collected from dams and fetuses and subsequently analysed for vitamin C. Fetal plasma and amniotic fluid concentrations showed negative associations with gestational age for both dietary groups, independent of an effect of dam (P < 0.001). A similar, though not significant, effect of gestational age was observed on placental vitamin C and group A fetal tissue concentrations. Fetal plasma, placental and amniotic fluid vitamin C concentrations were significantly higher in group B than group A (P < 0.001), suggesting the influence of maternal diet. Although the level of maternal vitamin C intake can influence the circulating concentration in the fetus, there is a decrease associated with increasing gestational age, independent of the maternal diet. The gestational age-dependent change in the fetal accumulation of vitamin C may reflect changes in the rate of placental transfer.

The effects of diet on the composition and properties of adipose tissue in relation to lymph nodes were studied in adult guinea-pigs. The proportions of monoenoic triacylglycerol fatty acids were constant in all sites in adipose tissue of similarly fed guinea-pigs, but were substantially greater in samples from guinea-pigs fed on suet-enriched chow. Triacylglycerols in adipose tissue from near nodes contained significantly fewer saturated fatty acids, and significantly more 18:2n−6 and 18:3n−3 than those in samples from sites remote from nodes within the same depot. Depots that interact most strongly with lymphoid cells in vitro had the largest and most consistent within-depot differences. The gradients of triacylgiycerol fatty acid composition with distance from lymph nodes in two small intermuscular depots were similar in guinea-pigs fed on plain or suet-enriched chow. These findings are consistent with the hypothesis that adipose tissue around lymph nodes is specialized for local interactions with the lymphoid cells therein, and help to explain the variability of serial or duplicate measurements of adipose tissue composition. When cultured alone, lipopolysaccharide-stimulated lymph node lymphoid cells from suet-fed guinea-pigs incorporated as much labelled thymidine as the controls. Adipose tissue explants from suet-fed guinea-pigs inhibited lymphocyte proliferation much less than those of the controls, although the site-specific differences were similar. The pattern of site-specific differences in glycerol released from explants incubated alone was generally similar for both dietary groups, but except in the popliteal depot, the increases following co-culturing with lymphoid cells were smaller for samples from suet-fed guinea-pigs. These experiments show that minor changes in the fatty acid composition of the diet can substantially alter the interactions between adipose tissue and lymphoid cells.

The purpose of this study was, first to explore metabolic interactions between Cu and ascorbic acid in guinea-pigs, particularly with respect to any possible disadvantages of high ascorbatein the presence of low Cu intakes, and second, to test the hypothesis that variations in ascorbate and/or Cu status might inhence collagen cross-linking, either by inducing a change in thecross-links: hydroxyproline ratio, or by inducing a change in the pyridinoline: deoxypyridinoline cross-linls ratio. Four matched groups, each of eight male weanliig Dunkin-Hartley guinea-pigs, were maintained on purified diets containing either no added Cu, or 150 mg Cu/kg diet, and either 0·1 g or 30 g ascorbic acid/kg diet. They were then killed 8 weeks later, and the following indices were measured body and organ weights; blood haemoglobin; adrenal ascorbate concentrations; Cu concentrations in plasma, liver and femur; superoxide dismutase (EC 1.15.1.1) activity in whole blood and liver; hydroxyproline, pyridinoline and deoxypyridinoline in femur and in urine. The principal observations were: Cu intake significantly affected blood and tissue Cu concentrations and superoxide dismutase activity; and ascorbic acid intake significantlyaffected adrenal ascorbate levels and the deoxypyridinoline: pyridinoline cross-links ratio, especially in bone (femur). There was evidence of a significant interaction between ascorbateand Cu with respect to adrenal and plasma Cu concentrations, blood superoxide dismutase activityand body weights. We conclude that interactions between ascorbate and Cu at the functional level were present but modest, and that a new and potentially powerful functional index of ascorbate status may exist within the deoxypyridinoline: pyridinoliie collagen cross-link ratio.

A 60 % reduction in maternal feed intake is known to cause a reduction of approximately 20 % in biceps brachii fibre number in the guinea-pig fetus. This investigation was designed to isolate the dietary component responsible by reducing all dietary components to 60 % of the ad lib. level and supplementing the protein, carbohydrate or fat component to the level of the ad lib. intake. Fetal muscles were examined at 50 d gestation to determine numbers of primary and secondary fibres, and at term to determine total fibre number. Fetal and neonatal weights were reduced in all restricted groups (P < 0.05) when compared with ad lib. controls. At term this reduction was significantly less (P < 0.05) in the protein-supplemented group (20%) than in the 60 %-restricted and fat-supplemented groups (43%) and the carbohydrate-supplemented group (34%). Biceps brachii fibre numbers were reduced in the 60%-restricted and fat-supplemented groups by 14–16%, but fibre numbers were similar in control, protein-supplemented and carbohydrate-supplemented groups. Any reduction in fibre number was in the secondary fibre component of total fibre number. Therefore, biceps brachii fibre numbers were reduced only when maternal diets were deficient in both protein and carbohydrate.

The purpose of the present study was first to assess the extent to which unlabelled ascorbate in the diet of guinea-pigs can exchange with labelled ascorbate within their organs when the dietary intake is varied over a wide range, and second to determine whether the retention of label might be used to assess either the amount of ascorbate intake or its biological availability where these are not known. The retention of [14C]ascorbate in the body and in various organs of guinea-pigs were, therefore, measured following a 13 d period of graded dietary intakes of ascorbate. It was found first, that the amount of label retained in each of the organs, 13 d after the initial dose of labelled ascorbate, was much more closely related to the amount of ascorbate intake after labelling than to the intake (and tissue ascorbate levels) before and at the time of labelling. Second, most of the individual internal organs exhibited a constant relationship between the specific activity at 13 d and the dietary intake, except for brain which was flushed to a smaller extent. Third, in agreement with several previous studies a high proportion of the radioactive label in the tissues was found to be still present in ascorbate. The specific activity of column-purified ascorbate was very similar to the estimated specific activity in the crude extract, which implies that it may be possible to estimate specific activities (or stable isotope enrichments) at certain sites without rigorous isolation procedures. Fourth, the amount of radioactivity appearing in the urine 2 d before killing the animals was correlated with the amount of ascorbate intake and with tissue specific activities, suggesting that intakes (or bioavailability) might be predicted from the patterns of label-appearance in the urine

The α-tocopherol content of a number of different fetal, neonatal and maternal guinea-pig tissues was determined and compared with plasma and erythrocyte α-tocopherol values. During late gestation, the fetal liver appears to act as a storage site for α-tocopherol, the majority of which is released immediately following birth. In contrast, lung and brain vitamin E levels are relatively constant over the final period of gestation and during early neonatal life. The ontogeny of α-tocopherol in brain and lung was similar to that for erythrocytes while plasma α-tocopherol content varied considerably and did not accurately reflect tissue α-tocopherol status. Surprisingly, fetal and maternal lung α-tocopherol concentrations were similar at all time-points considered, whereas fetal liver α-tocopherol status was always considerably greater than maternal liver α-tocopherol content. These results, if representative of the human fetus, suggest that preterm infants may not have tissue α-tocopherol concentrations as low as previously assumed and that during the perinatal period erythrocyte α-tocopherol content is a more accurate indicator of tissue α-tocopherol concentration than plasma α-tocopherol content.