Themitochondrialmalate aspartate shuttle system(MAS)maintains the cytosolicNAD+/NADH redox balance, thereby sustaining cytosolic redox-dependent pathways, such as glycolysis and serine biosynthesis. Human disease has been associated with defects in four MAS-proteins (encoded by MDH1, MDH2, GOT2, SLC25A12) sharing a neurological/epileptic phenotype, as well as citrin deficiency (SLC25A13) with a complex hepatopathic-neuropsychiatric phenotype. Ketogenic diets (KD) are high-fat/low-carbohydrate diets, which decrease glycolysis thus bypassing the mentioned defects. The same holds for mitochondrial pyruvate carrier (MPC) 1 deficiency, which also presents neurological deficits. We here describe 40 (18 previously unreported) subjects with MAS-/MPC1-defects (32 neurological phenotypes, eight citrin deficiency), describe and discuss their phenotypes and genotypes (presenting 12 novel variants), and the efficacy of KD. Of 13 MAS/MPC1- individuals with a neurological phenotype treated with KD, 11 experienced benefits—mainly a striking effect against seizures. Two individuals with citrin deficiency deceased before the correct diagnosis was established, presumably due to high-carbohydrate treatment. Six citrin-deficient individuals received a carbohydrate-restricted/fat-enriched diet and showed normalisation of laboratory values/hepatopathy as well as age-adequate thriving. We conclude that patients with MAS-/MPC1- defects are amenable to dietary intervention and that early (genetic) diagnosis is key for initiation of proper treatment and can even be lifesaving.

No description available.

CoenzymeQ10 (CoQ10) functions as an electron carrier in mitochondria transporting electrons from CI and CII to CIII in the respiratory chain (RC) for normal cellular energy (ATP) production. Mutations in genes of a complicated and not yet well understood CoQ10 biosynthesis cause primary CoQ10 deficiency, a rare autosomal recessive mitochondrial disorder (MD) with diverse heterogeneous clinical phenotypes. Although the major function of CoQ10 is to serve as electron transfer molecule it furthermore possesses multiple metabolic functions which can result in secondary CoQ10 deficiency. Five main clinical phenotypes are associated with CoQ10 deficiency although distinct genotype-phenotype associations are still absent due to the limited molecular genetic diagnoses of most reported CoQ10 deficiency cases. A correlation was found between reduced levels of CoQ10 in muscle tissue and deficient CII + III RC enzyme activities in a South African patient cohort, the current indicators for potential CoQ10 deficiency. The aim of the study was therefore to identify nuclear-encoded mutations in genes associated with CoQ10 deficiencies in a cohort of South African patients diagnosed with respiratory chain deficiencies (RCDs). A high throughput target enrichment strategy was performed in order to identify previously reported and/or possible novel CoQ10-assosciated disease-causing variants using Ion Torrent next generation sequencing (NGS) and an in-house developed bioinformatics pipeline. The data obtained were compared to clinical presentations of the patients to interpret the results of the identified variants considered to be possibly pathogenic. Targeted genes associated with primary CoQ10- and secondary CoQ10 deficiency was successfully sequenced in 24 patients, identifying 16 possible disease-causing variants. Of these variants three compound heterozygous variants were identified in three patients in genes ETFDH, COQ6 and COQ7, which were considered to be pathogenic according to the available data provided. Further validation of these three variants supported its pathogenicity in at least two of these variants (ETFDH and COQ6). In conclusion: This study contributed to better understanding the aetiology of a South African cohort of patients diagnosed with MDs. It also highlighted the valuable role of NGS for such investigations, and furthermore identified areas in the biochemical and molecular diagnostic strategy where improvements could be made in the future. / MSc (Biochemistry), North-West University, Potchefstroom Campus, 2015

CoenzymeQ10 (CoQ10) functions as an electron carrier in mitochondria transporting electrons from CI and CII to CIII in the respiratory chain (RC) for normal cellular energy (ATP) production. Mutations in genes of a complicated and not yet well understood CoQ10 biosynthesis cause primary CoQ10 deficiency, a rare autosomal recessive mitochondrial disorder (MD) with diverse heterogeneous clinical phenotypes. Although the major function of CoQ10 is to serve as electron transfer molecule it furthermore possesses multiple metabolic functions which can result in secondary CoQ10 deficiency. Five main clinical phenotypes are associated with CoQ10 deficiency although distinct genotype-phenotype associations are still absent due to the limited molecular genetic diagnoses of most reported CoQ10 deficiency cases. A correlation was found between reduced levels of CoQ10 in muscle tissue and deficient CII + III RC enzyme activities in a South African patient cohort, the current indicators for potential CoQ10 deficiency. The aim of the study was therefore to identify nuclear-encoded mutations in genes associated with CoQ10 deficiencies in a cohort of South African patients diagnosed with respiratory chain deficiencies (RCDs). A high throughput target enrichment strategy was performed in order to identify previously reported and/or possible novel CoQ10-assosciated disease-causing variants using Ion Torrent next generation sequencing (NGS) and an in-house developed bioinformatics pipeline. The data obtained were compared to clinical presentations of the patients to interpret the results of the identified variants considered to be possibly pathogenic. Targeted genes associated with primary CoQ10- and secondary CoQ10 deficiency was successfully sequenced in 24 patients, identifying 16 possible disease-causing variants. Of these variants three compound heterozygous variants were identified in three patients in genes ETFDH, COQ6 and COQ7, which were considered to be pathogenic according to the available data provided. Further validation of these three variants supported its pathogenicity in at least two of these variants (ETFDH and COQ6). In conclusion: This study contributed to better understanding the aetiology of a South African cohort of patients diagnosed with MDs. It also highlighted the valuable role of NGS for such investigations, and furthermore identified areas in the biochemical and molecular diagnostic strategy where improvements could be made in the future. / MSc (Biochemistry), North-West University, Potchefstroom Campus, 2015

Previous epidemiological evidence from a number of studies supports the hypothesis that the risk of essential hypertension, coronary heart disease and non-insulin dependent diabetes is, in part, programmed by intrauterine nutritional status. An increasing number of human studies indicate that the developing kidney is particularly vulnerable to the adverse effects of fetal growth retarding influences. In animals growth retarding diets or other insults, which have an impact on the development of cardiovascular functions, also appear to impact upon nephron number. In this study, the feeding of a 9% casein diet to pregnant rats, a mild protein restriction, reduced nephron number in the offspring, which progressively declined with age compared to those exposed to an 1 8% control diet. At weaning low-protein exposed offspring had hypertension and evedence of renal insufficiency. On natural death, the kidneys from aged male rats exposed to both low-protein and control maternal diets had a higher incidence glornerulosclerosis and renal disruption than females. Supplementing the maternal 9% casein diet with 3% glycine, 1.5% urea and 3% alanine in the rat normalised nephron number in the offspring. Only the addition of glycinc in the maternal low- protein diet prevented the appearance of high blood pressure in the offspring. In this study it has been demonstrated that in humans, those of a low birth weight or ponderal index, a marker of fetal undernutrition, had evidence of increased glomerular permeability, but not elevated blood pressure at age 10. This association was not evident at age 12 or in a separate cohort of young adults. It is possible that hypertension and a reduced nephron reserve are not causally associated. The evidence from this thesis suggest that prenatal undernutrition may programme renal structure in later life, but that renal programming is not one of the primary mechanisms leading to hypertension

ABSTRACT Title: Relative Energy Deficiency in Female Collegiate Track & Field Athletes. Background: Energy deficiency and its consequences have long been studied in female athletes because of it’s potential for increasing risks of illness and injury. Sustaining an energy deficient diet while training and during competition may result in muscle loss and reduction in performance. Studies suggest that athletes competing in sports focusing on appearance or a lean physique are at high risk for energy deficiency. In 2014, the IOC developed the concept of ‘Relative Energy Deficiency in Sport’ (RED-S) to include new components not previously included in the Female Athlete Triad. A study has not yet been completed applying the RED-S paradigm in collegiate track and field athletes. Objective: The purpose of this study was to examine the prevalence of RED-S in female collegiate track and field athletes. It was hypothesized that the majority of collegiate track and field athletes experience RED-S. It was also hypothesized that a greater percentage of distance runners experience RED-S than other track and field athletes, including throwers, jumpers, and sprinters. The components of RED-S assessed were menstrual function, bone health, and energy expenditure. Methods: This study was a descriptive cross-sectional study, obtaining data through the use of a questionnaire and a relative energy expenditure index on a population of 12 female collegiate track and field athletes. Data were obtained through the use of a LEAF-Q questionnaire, a three-day food and exercise recall, and body composition analysis. Results: The 12 athletes were a combination of distance runners (n=5), throwers (n=2), and sprinters (n=5). Average subject characteristics were: age (20.6 ±1. 44 years), height (165.6 ±7.5cm), weight (63.58 ± 16.97kg), and body fat percentage (20.9± 7.2). Average energy intake over three days was 2146 kcal (±627), and the average predicted energy expenditure was 2380 kcal (±458). Average hours spent in a catabolic (52.8 ± 24.0), highly catabolic (37.5 ± 25.0), anabolic (19.2 ± 24.0), and highly anabolic state (12.4 ± 21.0). Subjects were in a negative energy balance state the majority of the days analyzed, and 75% of the population had at least one day of dietary recall below 45 kcal/kg FFM/day. Spearman’s rho analysis found a significant inverse correlation between Day 1 hours spent in optimal energy balance (± 400 kcal) and body fat percent (p=0.024, rs= -0.643), and significant positive correlation between Day 1 hours spent in optimal energy balance (± 400 kcal) and fat free mass percentage (p=0.03, rs=0.625). Spearman’s rho analysis also found an inverse correlation between Day 1 hours spent in an energy deficit (s= -0.626), and a positive correlation between Day 1 hours spent in an energy deficit and body fat percentage (p=0.026, rs=0.636). Seven out of twelve participants scored ≥ 8 on the LEAF-Q putting them at risk for RED-S. Conclusion: The study highlights the misleading effect of averaging multiple days of dietary recall on energy balance. When participant’s dietary recalls were assessed day by day the majority of hours were spent in a catabolic state, however when the three days of the recall were averaged the severity of the hours spent in a catabolic state lessened. The associations in this study are consistent with previous studies evaluating the relationships between energy balance deficits and body composition, indicating that longer duration spent in an energy deficit is associated with lower lean and higher fat mass. The findings from the LEAF-Q show that 58% of participants were at risk for RED-S, and half of all participants had or were experiencing menstrual dysfunction.

Thesis (MSc) -- Stellenbosch University, 1990. / ENGLISH ABSTRACT: The main aim of this workpiece was to establish the physiological parameters against which a vitamin Bu deficiency could be measured. A comparison between the hematological values of healthy patients and those suffering from pernicious anemia due to vitamin Bu deficiency was done. A specific case of pernicious anemia was used in the comparison of abnormal values to the values of normal healthy patients. The comparison consisted of blood analyses with the help of specified instruments, photomicrographs of bone marrow and blood smears and statistical data. A Coulter Counter Model ZF was used for the hematological analyses of blood, a radio-isotope assay for serum vitamin B u was done and photomicrographs were taken with a NIKON Microflex camera with photomicrographic attachments. The importance of vitamin Bu has been shown in this workpiece. With the use of techniques and certain instruments, the effects of a shortage of vitamin Bu has been shown. Analyses of the blood from normal ,healthy patients was compared to that of patients suffering from pernicious anemia. It was demonstrated that pernicious anemia is characterized by a low erythrocyte count, hematocrit (Het), hemoglobin (Hb) and vitamin Bu levels together with a higher mean corpuscular hemoglobin (MCH) and mean corpuscular volume (MCV). In severe cases of pernicious anemia these levels are extremely high or low as the case may be. Together with these values, the investigation of pernicious anemic blood and bone marrow smears revealed abnormally large erythrocyte precursors and fewer leucocytes than normal. Abnormally shaped cells, called macrocytes, were seen which was due to the disruption in deoxyribonucleic acid (DNA) synthesis caused by the vitamin Bu deficiency. This study produced a set of hematological reference values. The comparative study between healthy and pernicious anemic patients demonstrated a significant drop in serum vitamin B12 values during pernicious anemia. The hematological effect was illustrated by the Coulter Counter blood analysis results and the microscopic examination revealed the presence of megaloblastic erythrocytes, oval erythrocytes, pear-shaped poikilocytes and polymorphonuclear neutropbils with hypersegmented nuclei in blood smears I during vitamin B12 deficiency. This dianoses can be supported by the presence of megaloblasts and metamyelocytes in pernicious anemic bone marrow. / AFRIKAANSE OPSOMMING: Die hoof doel van hierdie werkstuk was om fisiologiese grense te bepaal waarteen 'n vitamien B12 tekort gemeet kan word. 'n Vergelyking tussen die hematologiese waardes van gesonde persone en die van pasiente met pernisieuse anemie wat ontstaan het as gevolg van 'n vitamien B12 tekort was uitgevoer. Die waardes verkry vanaf 'n spesifieke geval van pernisieuse anemie. was vergelyk met waardes vanaf normale gesonde persone. Hierdie vergelyking het bestaan uit bloed analises, fotomikrograwe van bloed en beenmurg smere en statistiese data. Die hematologiese bloed analises was met behulp van 'n Coulter Teller model ZF uitgevoer. 'n Radio-isotoop bepaling vir serum vitamien B12 was gedoen en fotomikrograwe was met 'n NIKON Microflex kamera geneem. Die belang van 'n vitamien B12 tekort was in hierdie werkstuk gedemonstreer. Die effek van hierdie tekort is deur die gebruik van sekere instrumente en tegnieke aangedui en die resultate hiervan is vergelyk tussen gesonde persone en pasiente met 'n vitamien B12 tekort. Hierdie studie het bevestig dat pernisieuse anemie gekenmerk word deur verlaagde eritrosiet, hematokrit (Het), hemoglobien (Hb) en vitamien B12 vlakke tesame met verhoogde gemene korpuskulere hemoglobien (GKH) en gemene korpuskulere volume (GKV) vlakke. Gedurende ernstige gevalle van pernisieuse anemie kan hierdie waardes uitermatig hoog of laag wees. Benewens hierdie waardes het die ondersoek van bloed en beenmurg gedurende vitamien B12 tekort, abnormale groot eritrosiet voorgangers en 'n verminderde hoeveelheid leukosiete getoon. Abnormale sel vorms was ook sigbaar a.g.v. die onderbreking in DNA sintese wat deur 'n vitamien B12 tekort veroorsaak word. Pernisieuse anemie word verkry wanneer daar 'n vitamien B12 en/of folaat tekort in die dieet is of wanneer hierdie vitamiene nie geabsorbeer kan word nie. Die teenwoordigheid van makrosiete, ovaal eritrosiete, peervormige poikilosiete en polimorfonuklere neutrofiele met hipergesegmenteerde keme in bloedsmere dui op 'n megaloblastiese anemie. Hierdie diagnose kan ondersteun word deur die aanwesigheid van megaloblaste en reuse metamielosiete in die beenmurg. Die bepaling van vitamien B12 en folaat vlakke in die bloed kan as addisionele bewysstukke vir 'n volledige diagnose dien. Gedurende hierdie studie is daar 'n stel hematologiese verwysingswaardes vasgestel. Die vergelykende studie tussen gesonde persone en pasiente met pernisieuse anemie het getoon dat daar 'n beduidende verlaging in serum vitamien B12 waardes gedurende pernisieuse anemie is. Die hematologiese effek was ook duidelik waameembaar in die Coulter teller se bloed analiese en mikroskopiese ondersoeke het die · teenwoordigheid van makrosiete, ovaal eritrosiete, peervormige poikilosiete en polimorfenuklere neutrofiele met hipersegmenteerde keme in bloedsmere aangedui. Hierdie diagnose kan ondersteun word deur die aanwesigheid van megaloblaste en reuse metamielosiete in die beenmurg. / This study was financially aided by a bursary from the CSIR.

No description available.

<p align="justify"><i>Note des Bibliothèques : la thèse du Dr Vanderpas a été défendue en 1991 mais il n'est techniquement pas possible d'indiquer cette date dans le logiciel Bictel/e.</i></p> <p align="justify"><u>Première partie</u> : Fonction thyroïdienne de la naissance à 7 ans chez les enfants d’un essai clinique de supplémentation d’huile iodée versus placebo à la femme enceinte.</p> <p align="justify">L’endémie goitreuse du Nord-Congo (République démocratique, ex-Zaïre) a fait l’objet d’un programme de santé publique de prévention du goitre et du crétinisme dans le cadre du Centre d’Etudes Médicales de l’Université Libre de Bruxelles pour les actions de coopération de 1974 à 1995. Le partenaire congolais était l’Institut de Recherche Scientifique et le Bureau National des Troubles dus à la Carence Iodée.</p> <p align="justify">Le présente travail s’inscrit dans ce contexte et analyse plus particulièrement la fonction thyroïdienne chez l’enfant de zéro à sept ans, dans la continuité d’un suivi d’un essai clinique pharmacologique randomisé et contrôlé (RCT, Randomised Clinical Trial) de phase 2 consistant à administrer une huile iodée (Lipiodol®) à des femmes enceintes se présentant à la maternité de Karawa. Cette cohorte de femmes enceintes a été précédemment étudiée par le Professeur Claude-Hector Thilly*.</p> <p align="justify">Chez les enfants nés de mères non supplémentées en iode, l’histoire fonction thyroïdienne se caractérise comme suit : <li>Une fonction thyroïdienne relativement stable au ours de la première année de vie par rapport aux valeurs de TSH et de T4 sériques du sang de cordon ; les moyennes de ces marqueurs biologiques sont clairement indicateurs d’un niveau de carence iodée par rapport aux normes d’une population d’enfants belges d’âge comparable (T4 sérique abaissée et TSH sérique élevée) ;</li> <li>Une aggravation des altérations de la TSH et de la T4 sériques au cours de la deuxième année de vie, aggravation qui se poursuit jusqu’à la quatrième année ;</li> <li>Un maintien de marqueurs biologiques de TSH et T4 sérique fortement altérés au moins jusqu’à l’âge de 7 ans (étendue d’âge étudiée).</li></p> <p align="justify">Dans cette région, le manioc est connu pour son rôle goitrogène, au travers de son contenu en glucosides cyanogènes, et il avait été précédemment démontré que le thiocyanate élevé des mères passait librement la barrière placentaire. Au cours de la première année de vie, lorsque les nourrissons sont essentiellement alimentés au sein, le thiocyanate sérique diminue fortement et se rapproche de valeurs observées chez des enfants d’autres régions non exposés au manioc. La dégradation de la fonction thyroïdienne au cours de la deuxième année de vie coïncide avec l’introduction du manioc dans l’alimentation. Pour une valeur de concentration urinaire en iode stable au cours des 7 premières années de vie, la prévalence de goitre et les variations de T4 et TSH sériques suivent celles du thiocyanate sérique. Cela est confirmé au travers d’une analyse multi-variée qui met en évidence l’association entre les valeurs moyennes de TSH et T4 et les concentrations urinaires en iode et en thiocyanate.</p> <p align="justify">L’administration intra-musculaire d’huile iodée prévient les altérations de la fonction thyroïdienne chez la mère (Thilly 1978), et cette protection s’étend chez l’enfant jusqu’à 24 mois, c’est-à-dire jusqu’à ce que l’allaitement maternel reste le principal apport nutritionnel. Au-delà de 24 mois, des altérations de la fonction thyroïdienne apparaissent chez certains de ces enfants (Elévation de la TSH et abaissement de la T4), et au-delà de 4 ans, la fréquence des altérations de la fonction thyroïdienne est aussi fréquente chez les enfants de mères traitées que chez les enfants de mères non traitées.</p> <p align="justify">Au vu de la fréquence fort élevée d’altérations de la fonction thyroïdienne entre 4 et 7 ans (2/3 ont une TSH anormalement élevée > 10 mU/L), seuls certains enfants présentent les stigmates d’une hypothyroïdie prolongée depuis le début de l’existence. Il apparaît qu’il y a lieu de distinguer des hypothyroïdies juvéniles de durée, de sévérité, et de timing différents. Si l’hypothyroïdie juvénile est aussi fréquente au-delà de 4 ans dans les deux groupes de l’étude, les stigmates cliniques d’hypothyroïdie persistante sont plus fréquemment observés chez les enfants nés de mères non supplémentées en iode que chez les autres. De plus, la sévérité des stigmates cliniques (degré d’arriération mentale ; importance du retard de développement statural) démontre que l’hypothyroïdie persistante s’est installée plus précocement chez ertains enfants nés de mères non supplémentées en iode que chez les autres. Dans les formes les plus sévères, l’évolution staturale et le niveau d’intelligence de ces enfants avec hypothyroïdie persistante sont compatibles avec le tableau clinique de crétinisme myxédémateux endémique décrits chez le sujet adulte par les Professeurs François Delange et Jacques Dumont.</p> <p align="justify"><u>Deuxième partie</u>: étude du métabolisme iodé chez les enfants hypothyroïdiens et mise en évidence de la carence combinée en iode et en sélénium.</p> <p align="justify">Certains enfants hypothyroïdiens le sont depuis longtemps (depuis la naissance, éventuellement), d’autres le sont transitoirement, sans que leur hypothyroïdie passagère ne laisse de séquelles évidentes en termes de retard statural ou d’arriération mentale.</p> <p align="justify">Ceux qui sont en hypothyroïdie persistante au-delà de 4 ans ont une fonction thyroïdienne altérée : lorsqu’on leur administre de l’iode, leur glande ne répond pas à cette correction de carence iodée, et ils demeurent profondément hypothyroïdiens. Ce phénomène de non réponse à la correction de la carence iodée n’estpas observé chez les enfants hypothyroïdiens plus jeunes : cela démontre qu’il y a, chez certains enfants, une perte progressive de la capacité fonctionnelle de la thyroïde à répondre à la supplémentation iodée. Ces sujets développent le tableau clinique de crétin myxédémateux endémique.</p> <p align="justify">On constate que l’hypothyroïdie juvénile recouvre un vaste spectre depuis les cas d’hypothyroïdie transitoire jusqu’aux cas d’hypothyroïdie irréversible, même après correction de la carence iodée.</p> <p align="justify">Sur base d’hypothèse physiopathologique de cette perte de capacité fonctionnelle de la thyroïde chez certains jeunes enfants, il a été proposé qu’une carence combinée en iode et en sélénium pourrait expliquer ce processus. Une telle carence combinée a été décrite dans notre travail dans la région goitreuse du Nord-Congo, et pas dans d’autres régions non goitreuses du même pays ou dans d’autres endémies goitreuses avec peu de crétinisme myxédémateux endémique (Soudan, Sénégal).</p> <p align="justify"><FONT size=1>*Thilly Claude-Hector, Delange François, Lagasse Raphael, Bourdoux Pierre, Ramioul L, Berquist Helen, Ermans André-Marie. Fetal hypothyroidism and maternal thyroid status in severe endemic goiter. Journal of Clinical Endocrinology and Metabolism.</FONT></P>

Kelpak®, a seaweed concentrate (SWC) prepared from the brown seaweed Ecklonia maxima (Osbeck) Papenfuss, improves overall plant mass and fruit yield in a variety of crops. The main active principals isolated from Kelpak® are cytokinins and auxins. Although these compounds are partly responsible for the growth promoting effect observed with Kelpak® application, they do not fully account for the complete effect of Kelpak® treatment. For this reason the focus has turned to polyamines (PAs) which are found in all cells of plants, animals and microorganisms, including eukaryotic algae. Polyamines also have growth promoting effects in plants. A study was carried out to investigate the PA levels in E. maxima and Kelpak® through a biennial cycle and to investigate if the PAs present in Kelpak® may have an effect on root growth, alleviating nutrient deficiency and the transport and accumulation of PAs in plants. To determine the amount of PA in the stipes, fronds and SWC prepared from E. maxima, samples were collected monthly over a two-year period (June 2009-June 2011). Extracts were benzoylated and quantified using a Varian HPLC. Putrescine concentrations ranged from 15.98-54.46 μg.g⁻¹, 6.01-40.46 μg.g⁻¹ and 50.66-220.49 μg.g⁻¹ DW in the stipe, fronds and SWC, respectively. Spermine concentrations ranged from 1.02-35.44 μg.g⁻¹, 1.05-26.92 μg.g⁻¹ and 7.28-118.52 μg.g⁻¹ DW in the stipe, fronds and SWC, respectively. Spermidine concentrations fell below the detection threshold. This is the first report of PAs being detected in a SWC. The seasonal pattern established for the stipe, frond and SWC followed the same trend over a biennial cycle. Polyamines accumulated in the seaweed tissue during periods of active growth and as a stress response elicited by rough wave action. This PA trend was similar to the cytokinin trend reported by MOONEY and VAN STADEN (1984b) for Sargassum heterophyllum which suggests that PAs play an important role in the hormone cascade during active growth. Routine monthly screening of Kelpak® carried out in the Research Centre for Plant Growth and Development indicated that Kelpak® consistently resulted in more rooting in the mung bean bioassay than the IBA control. The potential root promoting effect of PAs were investigated. Individually applied PAs did not increase rooting in the mung bean bioassay, but a synergistic relationship was observed between Put (10⁻³ M) and IBA (10⁻⁴ M). When applied together, rooting increased significantly above Put (10⁻³ M) and IBA (10⁻⁴ M) applied separately. The Put-auxin combination produced a similar number of roots to those treated with Kelpak®. It is possible that the PAs present in Kelpak® have a synergistic effect with auxins present in Kelpak® to promote root development and growth. Several physiological effects of Kelpak® and PAs on plant growth were investigated in a series of pot trials. Kelpak® significantly improved the growth of P- and K-deficient okra seedlings and masked the detrimental effects exerted by P- and K-deficiency. The application of PAs (10⁻⁴ M) significantly improved the seedling vigour index (SVI) of okra seedlings subjected to N-deficiency. The statistical difference was attributed to the N-containing growth regulators and polyamines being degraded and metabolized by the okra seedlings. Polyamine application did not alleviate P- and K-deficiency but increased root growth significantly in seedlings receiving an adequate supply of nutrients. It is likely that the additional PAs supported auxin-mediated root growth. A pot trial with okra plants was conducted to establish if the PAs in Kelpak®, applied as a soil drench or foliar application, are absorbed and translocated in a plant. Plants were also treated with Put, Spm, Spd to establish if PAs can be absorbed and translocated. Once the fruit had matured, plants were harvested and the endogenous PA content quantified by HPLC in the roots, stems and fruits. Applying PAs as a soil drench was not as effective as a foliar spray at increasing the PA content in the different plant parts. Kelpak® treatment (0.4%) did not contribute more PAs in any plant part. Spermidine concentrations were higher, in the various plant parts, than Put or Spm, irrespective of the mode of application. The application of Put, Spd and Spm increased Spd concentrations in the roots. Considering that Spd is the main PA produced in the roots and that exogenously applied PAs are readily converted to Spd, it seems evident that Spd is the preferred PA for long-distance transport in plants. The cytokinins and auxins in Kelpak® play an important role in stimulating growth in plants. It is, however, the totality of different compounds in Kelpak® that gives it its unique growth stimulating ability. Polyamines, occurring within the seaweed contribute to this activity, having an active role in root production and thus increased plant growth. / Thesis (M.Sc.)-University of KwaZulu-Natal, Pietermaritzburg, 2011.