摘要:

SUMMARYPhotosynthetic bicarbonate assimilation and cation transport by aquatic plants are reviewed. It is suggested that these two processes stand in a causal relation to one another. A number of observations of cation transport not directly associated with photosynthesis are also reviewed, and are related to current concepts of active transport in the plant kingdom.These characteristics of cation transport have been observed in many submerged aquatic plants:1Cations are transported through the leaves in the light but not in the dark.2Cations are accumulated at the abaxial leaf surface from the contiguous external medium and are excreted from the adaxial surface into the medium. Therefore accumulation and excretion can be studied separately.A new theory of cation transport in bicarbonate‐assimilating aquatic plants is presented. The theory entails the following propositions:1Two active membranes pump cations through the leaf in the light. The membrane on the abaxial leaf surface pumps cations into the leaf; that on the adaxial surface pumps cations out of the leaf.2The cell plasma membranes on the abaxial and adaxial leaf surfaces form these two active membranes.3In the light–i.e. when the transport mechanism is functioning–the biochemical reactions of transport reach steady‐state levels. These levels are determined by the rates of reaction between the constituents. One can therefore alter the steady‐state levels by suitably altering the conditions of one or more of these reactions.4In the dark–i.e. when the transport mechanism is not functioning–the biochemical constituents reach equilibrium levels. The equilibria can be altered by changing the environment of the leaf.5The reactions of transport supply links of a respiratory chain.6The reactions of transport synthesize a bicarbonate‐accepting compound at the plasma membrane.Evidence for each of these propositions is discussed.The theory is considered applicable, with appropriate modification, to cation transport in a v

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1956.tb01555.x

出版商:Blackwell Publishing Ltd    

年代:1956

数据来源: WILEY

摘要:

SUMMARY1The hormones of crustaceans may be grouped into those which control effector organs (chromatophores, muscles) and those which control the more gradual sequences of growth, development and reproduction; they have been termed energetic and metabolic hormones respectively. Most of the known crustacean hormones originate in neurosecretory centres in the central nervous system.2The sinus gland is an important part of an elaborate neurosecretory system in the eyestalk of stalk‐eyed crustaceans and in the head of sessile‐eyed forms. It is largely composed of the swollen terminations of neurosecretory fibres. Some cellular elements have also been detected, but it is not yet known whether they have a secretory function. It is generally accepted that the greater part of the secretory material in the sinus gland has been transported thither along axon fibres from cell bodies in the central nervous system, though it has been suggested that the staining reactions of the sinus gland indicate also the probability of chemical transformation, if not autochthonous secretion. After‐sinus gland ablation the cut stump of the nerve leading to it continues to accumulate secretory material.3An indiscriminate use of the term X organ in the eyestalk has led to confusion. The X organ, originally described in detail by Hanstrom, is characterized by its association with a sensory papilla and by its contained concentric‐layered structures, here called ‘onion bodies’. The term X organ has been used by some authors to denote a group of neurosecretory cell bodies, the fibres of which terminate in the sinus gland. It is suggested that the sensory papilla X organ (Hanstrom's X organ) should be distinguished from the other X organs as it differs from them morphologically and physiologically.4The post‐commissure organs comprise enlargements of the epineurium of two post‐commissure nerves, containing the terminations of neurosecretory fibres. They have been shown to contain chromactivating hormones.5The pericardial organs comprise epineurial enlargements containing fine‐fibre terminations. They lie in the pericardial spaces and have been shown to contain substances active on the heart.6The Y organ, a glandular structure which contains hormones affecting the rate of development, is located in the antennary segment of those forms which have a maxillary excretory organ and in the second maxillary segment of those which have an antennary excretory organ.7Various groups of neurosecretory cells have been detected in the brain and in thoracic ganglia.8The term neurohaemal organ has been proposed to denote those tissues, through which substances produced in neurosecretory cells gain ready access to the blood.9The pigment pattern of any one crustacean species is fairly constant, but patterns differ in the different groups. The pigments are contained in monochromatic, dichromatic, trichromatic and tetrachromatic chromatophores. The chromactivating substances which have so far been separated from tissue extracts seem to act differentially on these chromatophore types.10The sinus glands and the post‐commissure organs contain a substance, found also in the corpora cardiaca of insects, which concentrates the red pigments in the large red and small red chromatophores ofLeander serratus;it has been called the A‐substance. When tissue extracts containing the A‐substance have been allowed to stand for some time the A‐substance disappears and is replaced by one or more substances which affect the red pigment in the small chromatophores but not that in the large chromatophores.11The post‐commissure organs contain, in addition to the A‐substance, a substance B which disperses red pigments, and also an A'‐substance which concentrates white chromatophore pigments and at the same time the red pigments of the large red chromatophores.12A substance which disperses black pigments in the chromatophores of crabs has been found in a great number of different crustacean species. It is present in the Natantia, but its function in these forms is not yet known.13There is some evidence that light may affect chromatophore and eye pigments directly, possibly by sensitizing them to chromactivating hormones.14Chromatophore and eye pigments continue to migrate rhythmically even if animals are kept in constant darkness or under constant illumination. One such rhythm inUcahas been shown to be in synchrony with the solar cycle, another with the lunar cycle. The rhythms seemed to be largely independent of temperature, and of the eyes and sinus glands.15The migration of distal retinal pigment appears to be controlled by one or two substances originating in the sinus glands; there is some evidence that the proximal and reflecting pigments may be influenced by hormones originating outside the sinus glands.16A heart‐accelerating substance found in the pericardial organs is without effect on the chromatophores.17The sinus glands release a diabetogenic principle which maintains the blood‐sugar level above a certain minimum. This substance appears to be released in response to stressing agents. In crabs, centres outside the eyestalk may also produce the hormone. The eyestalks seem to exert some measure of endocrine influence over glycogen metabolism, though this may be indirect.18There is some evidence that the eyestalks are implicated in an endocrine control of chitin formation and the decomposition of lipoids and carotenoids. The evidence for the hormonal control of protein metabolism is suggestive but incomplete.19Removal of the eyestalks has been shown to affect respiratory metabolism, and tissue homogenatesin vitrocan be affected by eyestalk extracts and by extracts of the sinus glands or of the central nervous system. Respiratory data in crabs deprived of their sinus glands suggest that a hormone controlling oxygen consumption is released at the sinus gland, though formed elsewhere.20There is evidence that a sinus‐gland principle influences calcium metabolism, but that this may only be effective in the winter non‐moulting season in those animals which moult annually. The phosphate content of the tissues and the blood changes cyclically with the calcium content and there is some evidence of endocrine control, though the substance appears to be different from that which affects calcium metabolism.21The eyestalk appears to contain an antidiuretic and water‐balance regulating hormone. It seems likely that this differs from the ‘moulting hormone’, although their actions seem to be very closely co‐ordinated.22The moulting cycle is under the control of at least three hormones and possibly as many as six. The moult‐inhibiting hormone of the eyestalk and brain inhibits the onset of the premoult, the period of preparation for moulting; the moult‐accelerating hormone accelerates and correlates the processes of the premoult once this has begun. Both these hormones may act upon the Y organ, which itself produces a hormone necessary for the moult process. The amount of water taken in at moulting is regulated by the water‐balance hormone of the eyestalk.23Ovarian growth is controlled, in both Natantia and Reptantia, by an ovarian‐inhibiting hormone emanating from the eyestalk.24Testicular growth is controlled in Brachyura, but not in those Natantia so far investigated, by a testis‐inhibiting hormone emanating from the eyestalk.25The ovary of some Malacostraca may secrete a progestational hormone responsible for promoting the development of the brooding characteristics.26The vas deferens gland in Amphipoda secretes a hormone controlling the development of the male secondary and accessory sexual characteristics.27Some colour‐change hormones and substances which affect the heart beat have recently been separated by chromatography and electrophoresis. Preliminary studies indicate that at least one of the colour‐change hormones contains peptide bonds which are necessary for its activity; one of the active substances in pericardial organ extracts is closely related to 5‐hydroxytryptamine. It is sug

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1956.tb01556.x

出版商:Blackwell Publishing Ltd    

年代:1956

数据来源: WILEY

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1956.tb01557.x

出版商:Blackwell Publishing Ltd    

年代:1956

数据来源: WILEY

摘要:

SUMMARY1I employcancerin a broad sense to cover all products ofmalignant neoplasia– carcinomas, sarcomas, leukaemias and ascites tumours–andtumourto cover all autonomous neoplasms.2Cancer is not a biological entity, but an assemblage of many distinct diseases (malignant tumours) which share the following symptoms: (a)replication of abnormal tissue type, but often with change towards greater malignancy;(b)non‐limited proliferation;(c)some degree of histological and physiological dedifferentiation;(d) partial or often complete lack of organization; (c) invasiveness, often accompanied by metastasis.3Neoplasiaalso includes the development ofbenign tumours, which exhibit symptoms(a)‐(d)above, and have therefore acquired autonomy.4Neoplasia does not involve an abnormal form of tissue differentiation, but a characteristic deviation of metabolism which may affect any type of tissue. Tumours retain the specific determination of the tissues from which they arise, though in hypoplastic manifestation. Tumorigenic metabolic deviation proceeds by a series of individual chance (mutational) events, instead of by a continuous (statistical) process affecting all cells simultaneously as in normal differentiation.5All autonomous neoplasms can be regarded as the equivalents of new biological species.6Though the tumours of lower vertebrates, invertebrates and plants often differ in various ways from those of mammals and birds, there is no reason for regarding them as irrelevant to the human cancer problem. They are autonomous and often malignant neoplasms, and have sometimes been experimentally induced.7Neoplastic tumours, whether spontaneous (in nature) (S), experimentally induced (E), or genetically induced (G), have been recorded in the following groups of organisms:8The ‘cancer spectrum’ may differ markedly in different groups, species and breeds.9High cancer‐proneness exists in some animal species (e.g. dogs, mice, budgerigars, domestic fowls, poecilid and cyprinodont fish) and breeds (retrievers, grey horses, some domesticated goldfish), and low cancer‐proneness in others (guinea‐pigs, rabbits, pigs, primates; Pekinese, chows).10Thyroid tumours develop frequently in salmonids and some other fish in water of low oxygen content. Their invasiveness is usually not an effect of malignancy, but of the absence of a capsule in the fish thyroid.11Attention is drawn to the favourable material for cancer research provided by regions of high localized growth rate (horns, horn cores, antlers, etc.), growth gradients (crustacean appendages and abdomina, molluscan mantle edges, etc.), endocrine‐dependent growth and regression (fowl‐combs, larval and metamorphosing Amphibia, stick insects, etc.), nerve‐dependent differentiation (Orthoptera), regenerating limbs (Amphibia, Crustacea, stick* insects, etc.), late‐fertilized Amphibian eggs, graft‐tolerant sites (cheek pouches of hamster), crown‐gall tumours and other plant galls, and toadstools.12The rate of development of spontaneous and induced tumours is related to size of species. Further investigation is needed to determine(a)if this holds also for size of breed,(b)if it is related to rate of development to maturity, or to length of life.13Crown‐gall tumours in plants are initiated by a bacterium,Agrobacterium tumefaciens, which induces an irreversible alteration in the plant's tissue leading to high heteroauxin production and unorganized tumorous growth. Plant tissues cultivated for long periods on media of high auxin content acquire many properties of crown‐gall tumour tissue. Desoxyribonucleic acid extracts fromA. tumefacienscan transform other species of bacteria so that they induce tumours.14Virus tumours in plants are induced by a combination of a specific virus and traumatic injury.15Some tumours are determined genetically, with high or complete penetrance, either as a result of gross genetic imbalance in species crosses(Nicotiana, Platy‐poecilus, Pygdera), or of chromosomal imbalance (extra B‐chromosomes inSorghumpollen‐grain tumours) or of single genes or systems of genes(Drosophilalarval melanotic tumours, melanomas in grey horses, human xeroderma pigmentosum, tumour incidence in monozygotic twins, some mammary cancers and leukaemias in mice).16The incidence (penetrance) of genetic tumours may vary markedly with diet and other environmental conditions (notably inDrosophila), with stage of development (allDrosophilatumours regress at metamorphosis), and with genetic background (notably in different inbred mouse strains, which show marked differences of proneness to various tumours). Some single genes affect cancer‐proneness, e.g.yellowin mice increases the incidence of lung cancer, and theAblood‐group allele in man that of gastric cancer.17Specific, subspecific and breed differences in cancer spectrum or particular cancer‐proneness must have a genetic basis; human ‘racial’ differences may do so, but may be determined by environment or habits.18The incidence of some mammary cancers in mice depends on a combination of genetic factors with a virus transmitted in the milk. Incidence is mediated through the timing of the endocrine‐dependent mammary cycle, high incidence occurring in strains where local areas of proliferation persist after the rest of the gland is in regression.19Histocompatibility genes determine susceptibility to tumour transplantation, but have no relation to genetic cancer‐proneness.20The study of ascites tumours has revealed a wide genetic variance in the cell populations of tumours, due to polyploidy, aneuploidy, structural changes (notably translocations) and gene mutations. The tumour is propagated mainly through a ‘germplasm’ of modal'stem cells’, the remaining more extreme variants constituting its non‐transmitted ‘soma’. In changed conditions, selection may operate to alter the profile (idiogram) of the variance, with the establishment of a new mode and set of stem cells (e.g. hypertetraploid in place of hyperdiploid). Major physiological adaptation of the entire cell population is not operative. Immunoselection results in new aneuploid modes with loss of antigenic properties. In other conditions, selection of other mutants may result in higher proliferation rate or invasiveness. Inbred mouse strains may change their general or particular cancer‐proneness, as a result of deliberate or unconscious selection. Thus, though the abnormal ploidies and structural changes often seen in tumours are certainly not the primary cause of tumorigenesis but secondary effects of it, they may provide the basis for further genetic evolution of the tumour.21The apparent lack of any marked ‘heredity’ of cancer in man and wild animal species is due to(a)the multiplicity of types of cancer, and(b)the genetic heterogeneity of natural populations. Whenever inbreeding is practised, breeds or strains with particular degrees of genetic proneness to particular cancers will be established. The high variance of human populations in genetic cancer‐proneness accounts for the fact that very high incidence of known occupational, environmental or habitudi‐nal cancer will only occur with very prolonged and very intense exposure to the carcinogen. Lesser degrees of exposure will result only in a moderate incidence, which yet may be causally significant, as with the increase of lung cancer due to cigarette smoking.22Evolutionary selection may affect the manifestation and incidence of cancers in various ways. It may operate(a)to produce a relative immunity to tumorigenesis in tissues especially subject to environmental insults, e.g. the nasal mucosa;(b)to defer the onset of reasonably common cancers, such as most carcinomas, to post‐reproductive ages; this will not be possible with rare cancers such as most sarcomas, or with cancers with very early onset, such as the leukaemias of childhood, or xeroderma pigmentosum; in this latter case selection has produced an alternative mode of palliation, by imposing recessiveness on the deleterious effects of the gene responsible.Cancers are also subject to a general orthoselec

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1956.tb01558.x

出版商:Blackwell Publishing Ltd    

年代:1956

数据来源: WILEY

ISSN:1464-7931    

DOI:10.1111/j.1469-185X.1956.tb01559.x

出版商:Blackwell Publishing Ltd    

年代:1956

数据来源: WILEY