Previous studies showed that spermine could protect the organism from oxidative damage in vivo. However, in vivo information on the antioxidant-related underlying molecular mechanism of spermine is limited. In this experiment, we further evaluated the effects of spermine supplementation and extended spermine administration on the antioxidant status and antioxidant-related signaling molecules gene expression in the liver and longissimus dorsi of piglets. A total of 80 piglets were randomly distributed to two groups, that is, those with adequate nutrient intake administrated with spermine (0.4 mmol/kg BW) or those with restricted nutrient intake supplemented by saline. The piglets were fed in pairs for 7 h or 3, 6, or 9 days. The results are as follows: (1) spermine can promote the antioxidant capacity by increasing enzymatic antioxidant capacity, glutathione content and clearance of oxygen radicals; (2) spermine significantly increased the mRNA levels of enzymatic antioxidant substances, NF-E2-related nuclear factor 2, Kelch-like ECH-associated protein 1, and the mammalian target of rapamycin but decreased the mRNA levels of ribosomal p70 S6 kinase in the liver and longissimus dorsi of the piglets.

Paraquat is known to affect all green plants and other eukaryotic organisms including mammalian cells. The aim of this study was to improve the understanding of paraquat toxicity in nonphotosynthetic plant cells using dark-grown kidney bean cells in tissue culture. It is shown that uptake of paraquat is an active process, and that paraquat inhibits cell growth, reduces DNA synthesis, and inhibits the activity of hydroxypyruvate reductase while enhancing the activity of glutathione reductase which is involved in cellular defense against oxidant stress. Additionally, it is demonstrated that iron ions are involved in paraquat toxicity. We conclude that uptake of paraquat into cells is via polyamine channels and that the deleterious effects of paraquat on these nonphotosynthetic cells are mediated by iron.

Polyamines are polycationic molecules that contain two or more amino groups (–NH3+) and are present in all eukaryotic and prokaryotic cells. Polyamines are synthesized from arginine, ornithine, and proline, and from methionine as the methyl-group donor. In the traditional pathway for polyamine synthesis, arginase converts arginine into ornithine, which is decarboxylated by ornithine decarboxylase (ODC1) to generate putrescine. The latter is converted to spermidine and spermine. Recent studies have indicated the existence of ‘non-classical pathways’ for the generation of putrescine from arginine and proline in animal cells. Specifically, arginine decarboxylase (ADC) catalyzes the conversion of arginine into agmatine, which is hydrolyzed by agmatinase (AGMAT) to form putrescine. Additionally, proline is oxidized by proline oxidase to yield pyrroline-5-carboxylate, which undergoes transamination with glutamate to produce ornithine for decarboxylation by ODC1. Intracellular production of polyamines is controlled by antizymes binding to and inactivating ODC1. Polyamines exert effects that include stimulation of cell division and proliferation, gene expression for the survival of cells, DNA and protein synthesis, regulation of apoptosis, oxidative stress, angiogenesis, and cell–cell communication activity. Accordingly, polyamines are essential for early embryonic development and successful pregnancy outcome in mammals. In this paper the main concepts on the history, structure and molecular pathways of polyamines as well as their physiological role on angiogenesis, and reproductive physiology are reviewed.

Maternal milk is the first source of exogenous polyamines for the newborn. Polyamines modulate gut maturation in neonates, but no studies are available on polyamine concentration in human milk of preterm babies, even though they could be important for their immature gut. The present study aimed to determine polyamine concentration in human breast milk of mothers with preterm or term infants during the first month of lactation. Human milk samples were obtained during the first month of lactation from twenty-seven mothers with preterm babies and twelve mothers with babies born at term. The polyamine concentration in human milk was quantified by HPLC. During the first month of lactation, the total polyamine concentration was significantly higher in preterm milk than in term milk samples (7590 (sd 4990) v. 4660 (sd 4830) nmol/l, respectively (P =0·034)), as well as individual polyamine concentrations. Polyamine concentration in mature milk for preterm babies was significantly higher than that in mature milk for babies at term, and a similar trend was observed in colostrum and transition human milk. The spermidine/spermine ratio was higher in transition milk in preterm v. term samples, while in mature milk, the ratio was significantly lower in preterm than in term babies. In conclusion, the polyamine concentration was significantly higher in human milk for preterm than for term infants. This and the different spermidine/spermine ratios could influence the gut development of premature babies.

A recombinant protein (approximately 38 kDa by SDS/PAGE), induced by expression in Escherichia coli of a cDNA encoding a 1-aminocyclopropane-1-carboxylate oxidase (ACO) isolated from embryonic axes of Cicer arietinum, was recognized by an antibody raised against an apple ACO. A monoclonal antibody, obtained from recombinant ACO of chick-peas, was used for immunolocalization experiments in the embryonic axes of chick-pea seeds. The results indicate that most of the ACO was present in the apoplast of the cell wall. No evidence of this protein in the vacuole was detected. During germination of C. arietinum seeds, the production of ethylene was induced in the embryonic axis; its highest value was reached when radicle emergence occurred. At this moment there was an accumulation of 1-aminocyclopropane-1-carboxylate (ACC), transcription of ACO mRNA, as well as maximal ACO activity. In the post-germinative period the activity of the last step of ethylene biosynthesis decreased. This decrease was eliminated by indole-3-acetic acid (IAA), which caused significant transcription of ACO mRNA. It is suggested that gene expression of ACO may be induced by auxins and spermine (Spm) and inhibited by abscisic acid (ABA).

The objective of this study was to investigate the effect of orally administered spermine at various doses on intestinal maturation in sucking piglets. Thirty-six 11-day-old sucking piglets were assigned randomly to one of six treatments to receive via a stomach tube 0, 0·1, 0·2, 0·3, 0·4, or 0·5 mmol spermine per kg live weight (LW) per day for 3 days. At day 14 of age, duodenum, jejunum and ileum were obtained for biochemical and morphological analysis. Increasing the dose of orally administered spermine increased intestinal weight (linear effect, P<0·01), mucosal weight (linear effect, P<0·05), and mucosal protein, DNA and RNA contents of the duodenum (linear effect, P≤0·01) and jejunum (linear effect, P<0·01). Elevating spermine doses also enhanced (linear effect, P≤0·02) the specific activities of maltase and sucrase but decreased (linear effect, P<0·01) lactase specific activity in the jejunum and duodenum. Furthermore, augmenting oral doses of spermine increased crypt depth and villus width but reduced villus height in the jejunum (linear effect, P<0·05) and duodenum (linear effect, P<0·01). For most measurements, the effects were observed at the oral spermine doses of 0·3 to 0·5 mmol/kg LW per day. Collectively, the results show that oral administration of optimal doses of spermine to 11-day-old sucking piglets induces precocious intestinal maturation and promotes intestinal growth.

The objective of this study was to determine the effect of stage of lactation on the concentration of polyamines (spermine, spermidine, and putrescine) in sow colostrum and milk. Ten, third parity sows (Landrace×Yorkshire) were sampled throughout a 28-day lactation. Litter size for all sows was standardized at 10 sucking piglets immediately after farrowing. Colostrum collection began at the birth of the first piglet (0 h), and colostrum was subsequently collected 6, 12, 18, and 24 h after farrowing. Sow milk was sampled on days 3, 7, 10, 14, 17, 21, 24 and 28 of lactation. Spermine concentration in sow colostrum was relatively constant for the first 12 h after farrowing and then rapidly increased to 10·26 μmol/l 24 h after farrowing (linear and quadratic effect; P<0·01). In contrast, the concentrations of spermidine and putrescine showed little change during the first 24 h with spermidine concentration in colostrum ranging from 3·76 to 4·54 μmol/l, and putrescine concentration ranging from 1·15 to 1·52 μmol/l. The highest concentration of spermine in sow milk was 18·82 μmol/l, observed on day 7, with levels gradually declining to 4·28 μmol/l by day 28 of lactation (linear and quadratic effect; P<0·01). In contrast, the concentration of spermidine increased during lactation ranging from a low of 4·32 μmol/l on day 7 to a high of 9·01 μmol/l on day 28 of lactation (linear effect P<0·01; quadratic effect P=0·03). Putrescine concentration ranged from 1·53 μmol/l on day 3 to 1·84 μmol/l on day 28 (linear effect P=0·07; quadratic effect P>0·05). The results of this study show sow colostrum and milk provide polyamines for sucking piglets before weaning, which could potentially modulate intestinal maturation.

We questioned whether polyamines coming from the diet or produced by intestinal microflora or by intracellular metabolism influence intestinal functions. Therefore, we compared pathogen-free rats and germ-free rats receiving a diet with low polyamine content and either treated or not treated with difluoromethylornithine (DFMO) and/or methylglyoxal bis (guanylhydrazone) (MGBG). Wet weight, protein content, DNA content, sucrase (EC3.2.1.48), maltase (EC 3.2.1.20) and lactase (EC 3.2.1.23) specific activities, amounts of putrescine, spennidine and spemine were measured in the mucosa of the proximal and distal intestine. Body weight was also determined. Rats without microflora had a higher specific activity of maltase and higher amounts of spermidine and spermine but lower lactase specific activity than pathogen-free animals; the low-polyamine diet given to gem-free rats had little effect on the functional variables measured (decrease of maltase and lactase specific activities) and did not modify the amounts of polyamines. DFMO and/or MGBG administered to germ-free rats receiving a low-polyamine diet induced modifications of most of the variables studied. Body weight and wet weight of proximal and distal intestine decreased, disaccharidase specific activities decreased, and amounts of polyamines changed according to the inhibitor used. Thus, our results showed that the deprivation of polyamine supply from microflora or from the diet failed, under our experimental conditions, to affect the intestinal properties analysed but exogenous and endogenous polyamine restriction altered general properties of the organism as well as intestinal functions.