Growth Hormone Supplementation Research Articles

O.27 Integrated hormonal and metabolic effects of recombinant human growth hormone (rhGH) supplementation in severely injured trauma victims

O.27 Integrated hormonal and metabolic effects of recombinant human growth hormone (rhGH) supplementation in severely injured trauma victims

Insulin-like growth factor-I gene expression in the tibial epiphyseal growth plate of growth hormone-treated uremic rats

To identify the molecular mechanisms involved in long bone growth of uremic animals, we evaluated the effects of recombinant human growth hormone (rhGH) supplementation on whole body growth, growth plate morphometrics, and insulin-like growth factor-I (IGF-I) gene expression in the tibial epiphyseal growth plates of uremic rats. Uremia was induced by a two-stage subtotal nephrectomy (Nx) of 30-day-old rats, followed by rhGH (N = 6) or saline (N = 6) treatment from day 56 to day 70 of age. Controls (N = 4) were sham decapsulated. Treatment with rhGH on Nx animals caused: (1) a significant increase in weight, (2) longitudinal growth similar to controls, and (3) increased total growth plate width predominantly due to an increase in hypertrophic zone width. rhGH increased IGF-I mRNA abundance in both zones, but the increase was greater in the proliferative zone. These changes were accompanied by concomitant alterations in IGF-I immunoreactivity. In uremic animals, therefore, rhGH treatment induces local IGF-I gene expression in the growth plate and increases the hypertrophic zone width but not the proliferative zone width. The latter suggests resistance to IGF-I action in that zone.

Effect of growth hormone and protein intake on tumor growth and host cachexia

Growth hormone supplementation has been shown to stimulate muscle protein synthesis and to improve nitrogen balance in a variety of catabolic states. The role of growth hormone to support the tumor-bearing host is complicated by the risk that growth hormone or its intermediaries may stimulate tumor growth. The purpose of this study is to examine the effect of growth hormone supplementation in tumor-bearing rats. This is studied in the protein-fed and protein-starved state in an attempt to isolate a selective benefit for the host over the tumor. Forty Lewis rats bearing a metastatic mammary adenocarcinoma (MAC-33) were divided into four groups: one receiving a regular diet plus saline solution, one receiving a regular diet plus growth hormone (1 IU/kg/day), one receiving protein-depleted diet plus saline solution, and one receiving a protein-depleted diet plus growth hormone. After 25 days of growth hormone treatment, animals were killed to determine primary tumor size, tumor/carcass ratio, host organ composition, pulmonary metastasis, and serum amino acid levels. The tumor/carcass ratio was decreased as a result of growth hormone treatment in both the protein-fed and protein-starved groups. Growth hormone supplementation resulted in increased carcass weight, muscle weight, and muscle protein content in the protein-fed, tumor-bearing animals (p < 0.05). In the protein-starved, tumor-bearing rats growth hormone supplementation resulted in a significant decrease in tumor volume and tumor protein content. Amino acid analysis suggests that the amino acid tyrosine is a rate-limiting substrate for tumor cell proliferation in this model. Growth hormone has a differential effect on tumor and host growth in the protein-fed and protein-starved state. Growth hormone supplementation inhibited tumor growth in protein-deprived animals. This is most likely accomplished indirectly by limiting amino acid substrate availability to the tumor.

Adjuvant growth hormone therapy in poor responders to in-vitro fertilization: a prospective randomized placebo-controlled double-blind study

The objective of the study was to assess the effect of growth hormone (GH) supplementation to a combined gonadotrophin-releasing hormone agonist/human menopausal gonadotrophin (GnRHa/HMG) treatment protocol on ovarian response in 'poor responders' undergoing in-vitro fertilization (IVF). GH or a placebo were administered in a prospective randomized double-blind manner. A total of 14 poor-responder patients (oestradiol < 500 pg/ml, less than three oocytes retrieved in two previous IVF cycles) were randomly allocated to a combined treatment of either GnRHa/HMG/GH (18 IU on alternate days, total dose 72 IU) or GnRHa/HMG placebo. No difference was found between the study and control groups in the number of HMG ampoules used, the number of follicles (> 14 mm) and serum oestradiol concentrations on the day of administration of human chorionic gonadotrophin (HCG), the number of oocytes retrieved and fertilized, and the number of embryos transferred. The GH group (n = 7) did not show a better ovulatory response in the study cycles; mean +/- SD serum oestradiol on day of HCG 411 +/- 124 versus 493 +/- 291 pg/ml, aspirated oocytes 2.2 +/- 1.5 versus 1.9 +/- 2.0. Interestingly, when the above results for the placebo group were compared with their previous cycles (serum oestradiol 403 +/- 231 pg/ml; 0.4 +/- 0.5 aspirated oocytes), a non-specific effect was found. Follicular recruitment, oestradiol secretion by mature follicles and the number of oocytes retrieved in poor responders were not improved by GH supplementation.

Effects of growth hormone administration in addition to gonadotrophins in normally ovulating women and polycystic ovary syndrome (PCO) patients.

Follicular fluid sex-steroids, insulin-like growth factor-I (IGF-I), IGF-I binding protein (IGF-I-BP) and epidermal growth factor were investigated in patients with polycystic ovaries and normally ovulating women, following ovulation induction with gonadotrophins or growth hormone plus gonadotrophins. Growth hormone supplementation enhanced the ovarian response to gonadotrophins, and significantly increased follicular fluid IGF-I in both groups, without affecting follicular fluid epidermal growth factor; growth hormone supplementation significantly decreased follicular fluid androstenedione in both groups.

The effect of growth hormone supplementation on in vitro fertilization outcome: a prospective randomized placebo-controlled double-blind study

To determine the effect of growth hormone (GH) supplementation to a long gonadotropin-releasing hormone agonist (GnRH-a)/human menopausal gonadotropin (hMG) treatment protocol, on ovarian response, embryo quality, and clinical outcome in in vitro fertilization (IVF). Growth hormone or placebo were administered in a prospective randomized double-blind manner. Forty-two normal ovulatory, women who were 38 years of age or less with mechanical factor infertility and a normal male factor were selected for this study. Gonadotropin-releasing hormone agonist, 0.5 mg/d, was initiated in the midluteal phase of the preceding cycle and continued until the day of human chorionic gonadotropin (hCG) administration. Ovulation induction with hMG was started 14 days after pituitary down regulation (17 beta-estradiol [E2] serum level less than 30 pg/mL). Growth hormone (12 IU/d) or placebo were administered on days 1, 3, 5, and 7 of hMG treatment. Breaking the code at the completion of the study revealed that 20 women received GH and 22 placebo. The age and duration of infertility did not differ between the two groups. Follicular phase duration, hMG ampules used, serum E2, and number of follicles (greater than or equal to 14 mm) on day of hCG as well as number of oocytes and embryos achieved were similar in both groups. Embryo morphology and rate of cleavage were also similar. Insulin-like growth factor-I (IGF-I) serum levels did not change after pituitary down regulation and increased significantly both after GH/hMG and placebo/hMG ovulation induction treatment. Clinical pregnancy rate (PR) per embryo transfer and implantation rate were 40% versus 32% and 17.9% versus 11.3% in the GH and placebo groups, respectively, and were not statistically different. In normo-ovulatory women undergoing ovulation induction for IVF, GH supplementation to hMG after GnRH-a pituitary down regulation does not seem to augment ovarian response or improve embryo quality. The effect of this regimen on actual PRs and implantation rates needs further clarification.

Effect of Thyroxine and Chicken Growth Hormone on Immune Function in Autoimmune Thyroiditis (Obese) Strain Chicks

The effect of thyroxine (T4) and/or recombinant chicken growth hormone (rcGH) supplementation on immune function and on immune cell maturation was examined in Obese strain chickens. Day-old Obese strain chicks received the control treatments or were treated with either T4 (supplemented in the diet), T4-rcGH, or rcGH (by daily injection) in a full factorial design. At 4 weeks of age, the proliferative activity of peripheral blood T cells to either mitogenic or allogenic cell (mixed lymphocyte response) challenge was assessed. At the same time, peripheral blood lymphocytes and thymocytes were collected and prepared for flow cytometry analysis. Proliferative responses to both T cell mitogens and allogeneic splenocytes were significantly increased (P less than 0.05) by rcGH treatment, while the combined T4-rcGH treatment resulted in a significant increase in allogeneic and in concanavalin A responsiveness, but not in the response to phytohemagglutinin. All supplemented groups showed a significant decrease in the mean fluorescent intensity for CT-1a+ thymocytes, while thymocytes from birds receiving either T4 or rcGH alone had higher proportions of CD4+ and CD8+ cells. The monoclonal antibody staining of thymocytes from T4-rcGH-supplemented animals more closely resembled that of the unsupplemented controls. Among the peripheral blood lymphocytes, there were no changes in the numbers of CD4+, CD8+, or sIg+ cells as a result of treatment. The mean fluorescent intensity of sIg+ cells was significantly decreased, however, as a result of T4 supplementation when given either alone or in combination with rcGH. Finally, the mean fluorescent intensity ratios of CD4+ to CD8+ cells was significantly increased as a result of rcGH supplementation. These results strongly support a role for both the thyroid hormones and growth hormone in regulating and/or enhancing immune function, with changes in functional responses paralleled by concomitant changes in the T cell populations as expressed by shifts in T cell surface marker expression.

Supplemental growth hormone alters body composition, muscle protein metabolism and serum lipids in fit adults: characterization of dose-dependent and response-recovery effects

Using double-blind, placebo-controlled procedures, the effects of low and high therapeutic dosages of methionyl-human growth hormone (met-hGH) on body composition, muscle protein metabolism and serum lipids were studied in 7 fit adults without growth hormone (GH) deficiency. Dose-dependent changes in body composition were observed that in part appeared to be influenced by a response-recovery effect, as measured by responses factored according to the duration of washout between exposure to the low and high dosages of met-hGH (6 weeks vs. 12 weeks vs. 18 weeks). Increases in fat-free weight were accompanied by an increase in skeletal muscle protein metabolism. Basal levels of cholesterol were inversely related to peak levels of GH in response to exercise stimulation and IGF-I, while GH supplementation lowered levels of total cholesterol and high- and low-density lipoproteins. A dose-dependent effect occured for total cholesterol, and the percent change in cholesterol was related to the percent change in insulin-like growth factor I (IGF-I). Endogenous levels of GH were attenuated in response to stimulation and IGF-I levels were increased after treatment with GH, but no dose-dependent changes were observed. We conclude that met-hGH alters body composition and muscle protein metabolism, and decreases stored and circulating lipids in fit adults with a preexisting supranormal body composition. The physiological profile of the person was not as important as the treatment conditions in determining the somatic and physiological response outcomes.

Immunoreactive human growth hormone like peptides in tropical Penaeids and the effect of dietary hGH onPenaeus vannameilarval development

Human growth hormone like peptides were present in Penaeus indicus as two molecular forms: one with a molecular weight about 25 kDa which is similar to that of the vertebrate growth hormone and a smaller form of 2 kDa. Quantitative variations of hGH-like peptides in different larval stages of three species of Penaeids (Penaeus vannamei, P. stylirostris, P. indicus) suggest a possible involvement of hGH-like peptides in the development. Human growth hormone (hGH) supplementation in the diet of Penaeus vannamei larvae seems to have a positive effect on the size and on the quality of the animals estimated by their resistance to salinity stress.

Influence of inorganic salts on cytokinin induced caulogenesis in leaf segments of Rosmarinus officinalis L.

The efficacy of cytokinin for caulogenesis (shoot bud differentiation) in leaf segments of Rosmarinus officinalis was greatly modified by inorganic salts of the medium. The presence of NH 4NO 3 and KNO 3 together was essential for the induction of shoot bud differentiation besides the growth hormone supplements. For optimum shoot bud differentiation with the minimum concentrations of 6-benzylaminopurine (BAP) and indole-3-acetic acid (IAA) (0.25 mg 1 −1 and 0.1 mg 1 −1, respectively), 1000 mg 1 −1 NH 4NO 3 and 1500 mg 1 −1 KNO 3 were found to be best. Similarly, the presence of other inorganic salts, except CaCl 2, of Murashige and Skoog's (1962) medium (MS) was essential for shoot bud differentiation as inhibition occured in the absence of any of the major salts (save CaCl 2) and of trace elements. Shoot bud differentiation was in fact inhibited by the presence of Ca 2+. The basal petiolar portion of a leaf showed the maximum regenerative potential followed by the median portion, while the tip had the least. The leaf-regenerated plants grew normally in soil under glasshouse conditions

Effect of Growth Hormone on Immune Function in Normal and Hypophysectomised Rats

The effect of growth hormone (GH) on immune function was studied using normal and hypophysectomised male Wistar rats. Hypophysectomy was performed by the auditory approach at 4 weeks of age. Normal and hypophysectomised rats were treated with saline or 0.4IU/body GH daily during 7 to 11 weeks of age. Histological features of the thymus and spleen and immunological parameters including blood cell counts, lymphocyte subsets, serum immunoglobulin levels, splenic natural killer activity, and mitogen-induced splenic lymphocyte proliferation were examined in the rats at 11 weeks of age. In hypophysectomised rats, the counts of peripheral white blood cells (5,513 +/- 813/microliters), lymphocytes (4,838 +/- 737/microliters), Th/i cells (2,237 +/- 329/microliters), and B cells (1,400 +/- 509/microliters), Th/i/Ts/c ratio (1.78 +/- 0.27), splenic T cell subsets (pan T: 51.0 +/- 4.3%, Th/i: 31.6 +/- 3.0%, Ts/c: 23.9 +/- 2.7%), and serum IgG level (2,148 +/- 470mg/l) were significantly decreased as compared with normal rats. Natural killer activity (17.8 +/- 4.6%) and mitogen-induced proliferation of T cells (Con A: 47.1 +/- 15.7, PHA: 51.6 +/- 12.5) were also suppressed. Hypoplasia of the thymus and spleen was observed in parallel to retarded growth of the rats. In contrast, GH supplement to the hypophysectomised rats resulted in increases in growth and lymphoid tissue, and the restoration of the counts of peripheral white blood cells (6,850 +/- 840/microliters), lymphocytes (6,211 +/- 731/microliters), Th/i cells (2,909 +/- 304/microliters), and B cells (1,947 +/- 402/microliters), Th/i/Ts/c ratio (2.04 +/- 0.34), serum IgG level (3,414 +/- 1,326mg/l), and natural killer activity (25.7 +/- 4.7%). However, splenic lymphocyte subsets and mitogen-induced proliferation of T cells were not recovered by GH treatment for 4 weeks. GH administered to normal rats increased serum IgG level (4,982 +/- 1,496mg/l) but did not affect other immunological parameters. These results indicate that humoral and cell-mediated immune function are impaired in hypophysectomised rats, but GH supplement administered to them restored most of the impaired immune function, suggesting that GH plays an important role in the development of immune function.

Lipid synthesis and lipoprotein secretion by chick liver cells in culture: influence of growth hormone and insulin-like growth factor-I.

1. Chick liver cells were incubated in unsupplemented medium (control), or medium supplanted with either 1 microgram/ml pituitary derived chicken growth hormone (GH), 50 ng/ml recombinant human insulin like growth factor-I (IGF-I), or 1 microgram growth hormone/ml and 50 ng insulin like growth factor-I/ml (GH + IGF-I). 2. GH supplementation stimulated acetate incorporation into liver cell lipid. Low density lipoprotein (LDL) lipid secretion was increased quantitatively by GH. 3. Cells incubated with IGF-I incorporated more acetate into lipid and secreted more lipid as VLDL and HDL than controls. 4. A metabolic antagonism between GH and IGF-I was evident with respect to lipogenesis. 5. Neither GH nor IGF-I altered, quantitatively, cell protein synthesis or apoprotein secretion.

Effects of Culture Conditions on Formation and Hormone Content of Fetal Porcine Isletlike Cell Clusters

To establish methods for stimulation of the growth and differentiation of fetal endocrine pancreatic cells, a technique for the in vitro production of fetal porcine isletlike cell clusters (ICCs) was used. By varying the composition of the culture medium with different glucose concentrations and the addition to the culture medium of insulin, growth hormone (GH), amino acids, or nicotinamide, we estimated the formation of ICCs and their hormone content. High glucose content (28.0 mM) stimulated the formation of abundant ICCs that contained decreased amounts of insulin. In contrast, culture at a low (5.6-mM) glucose concentration increased the ICC insulin content but decreased the number of ICCs formed. Addition of seven times the normal amount of amino acids hampered both the formation of ICCs and their insulin content. Neither insulin nor GH supplementation of the medium influenced the ICC insulin content, but GH stimulated an abundant outgrowth of ICCs containing relatively high insulin concentrations. However, ICCs formed under these circumstances contained less than 10% of the insulin content of adult islets, and further work has to be carried out to identify factors responsible for further differentiation of the fetal porcine pancreas.

Pre-adipocyte proliferation and differentiation in response to hormone supplementation of decapitated fetal pig sera.

Growth hormone and thyroid hormones have been implicated as important serum factors for adipocyte development in cell culture. Fetal decapitation removes these factors from serum of the growing fetal pig and results in development of fewer adipocytes than in intact fetuses. These experiments examined the effects of growth hormone or thyroxine supplementation to decapitated fetal pig sera upon pre-adipocyte proliferation and differentiation. Hormones were supplemented to concentrations present in sera from intact pig littermates (reference). Sera +/- hormones were analyzed for their effects upon pre-adipocyte proliferation as determined by [3H]-thymidine incorporation; enzyme expression as determined by sn-glycerol-3-phosphate dehydrogenase activity; and induction of complete differentiation into lipid filled adipocytes as based upon a pre-adipocyte proliferation and enzyme expression than reference sera. Growth hormone had no effect in decap sera upon these parameters. Decap sera permitted detection of 54% more lipid-accumulating, newly formed adipocytes on percol gradients than reference sera, but growth hormone reduced detection to 29% of reference sera. Thyroxine specifically stimulated pre-adipocyte proliferation more than decap sera, but not to the level of reference sera. Complete differentiation, a formation of lipid-accumulating adipocytes was promoted also by thyroxine in comparison to basal decap sera. The results of these experiments indicate thyroid hormones are an important component of fetal sera for regulation of adipocyte development, whereas growth hormone may only affect cellular metabolism and not promote pre-adipocyte growth and development.

Growth hormone and athletes.

Growth hormone is a powerful anabolic hormone that affects all body systems and plays an important role in muscle growth. It is released from the anterior pituitary in response to a variety of stimuli including exercise, sleep, stress, and the administration of a variety of drugs and amino acids. Serum levels are variable and are dependent on such factors as age, sex, body composition and level of fitness. Animal experiments have shown that growth hormone can partially reverse surgically induced muscle atrophy and weakness. Growth hormone administration to normal animals leads to muscle hypertrophy, but this muscular growth is not accompanied by increased strength. Growth hormone excess leads to acromegaly, a disease with significant morbidity, including a myopathy in which muscles appear larger but are functionally weaker. Although there is no scientific evidence documenting an improvement in athletic performance following growth hormone supplementation, it is reported that this practice is becoming more widespread among athletes wishing to avoid detection with current doping control measures. There are anecdotal reports that athletes are injecting cadaveric or biosynthetic forms of growth hormone, both of which are associated with potentially serious complications. In addition, some athletes are ingesting drugs and amino acids in the belief that their endogenous growth hormone secretion will be increased. There have been no scientific studies on the effects of growth hormone supplementation, and the anecdotal reports have been equivocal, with some individuals reporting spectacular results while others report no change. Despite the lack of valid evidence for its efficacy and its potentially serious side effects, it has been predicted that growth hormone use may increase. Growth hormone use and abuse has the potential to dramatically change the future conduct of athletics and may prove to be a threat to the concept of fair competition.

Growth hormone regulation of the expression of differentiation-dependent genes in preadipocyte Ob1771 cells.

The adipose conversion of Ob1771 preadipocytes, during exposure to medium containing bovine serum and supplemented with growth hormone, is accompanied by the acquisition of phenotypic markers and the increased accumulation of specific mRNAs. The expression of lipoprotein lipase, and that of unidentified pOb24 and pGH3 mRNAs, are early events which are independent of growth hormone supplementation. By contrast, the late expression of mRNAs encoding for glycerol-3-phosphate dehydrogenase and p422 protein (a myelin-P2 homologue) and that of glycerol-3-phosphate dehydrogenase activity require the presence of growth hormone. The abundance of beta-actin mRNA does not change during differentiation. Runoff transcription by nuclei isolated from untreated or growth hormone-treated cells reveal little or no change in the rates of transcription of pOb24, pGH3 and beta-actin mRNAs. By contrast, the transcription rate of the p422 gene increases markedly (greater than 6-fold) in nuclei of growth hormone-treated cells. However, the p422 mRNA is more abundant than would be predicted by its nuclear transcription alone, suggesting, in Ob1771 cells exposed to growth hormone, that there is a post-transcriptional level of control. These results indicate that the permissive role of growth hormone during adipose cell differentiation is related to terminal events only and that its effects can be seen both at the protein and mRNA level. These results strongly suggest that an increased rate of specific transcription is primarily responsible for the accumulation of mRNAs during exposure to growth hormone.

Studies on DNA, RNA and protein synthesis in Malathion treated germinating seeds ofVigna Sinenses(L): effect of plant growth hormone supplementation

Studies have shown that malathion causes differential inhibition in the uptakes of 14C‐uracil, 14C‐leucine and 3H‐thymidine, the radioactive precursors of RNA, protein and DNA respectively, when compared to the control seeds. The rate of RNA, protein and DNA synthesis were also found to be inhibited under malathion exposed conditions (above 50 ppm), in a dose dependent manner. On simultaneous application of either of the plant hormones, i.e. IAA (10‐4M), GA3 (10‐3M) or kinetin (10‐4M) at different concentrations of malathion, it was found that there was a trend to inhibit malathion action.

Pretranslational regulation of alpha 2u-globulin in rat liver by growth hormone.

Hypophysectomy is known to cause complete suppression of the hepatic synthesis alpha 2u-globulin. The effect of hypophysectomy on the synthesis of alpha 2u-globulin can be reversed by multiple hormone treatment. The role of pituitary growth hormone in the multihormonal regulation of alpha 2u-globulin in rat liver was examined in the hypophysectomized male rats with and without growth hormone supplementation. Daily treatment of hypophysectomized rats with 5 alpha-dihydrotestosterone, corticosterone, thyroxine, and growth hormone for 8 days caused about 80% recovery in the hepatic content of alpha 2u-globulin and its corresponding mRNA as determined by radioimmunoassay, in vitro translation, and liquid hybridization with a cloned cDNA probe. However, omission of growth hormone from the treatment regimen failed to raise hepatic alpha 2u-globulin and its mRNA to more than 5% of the normal control. The possible effect of growth hormone on the translation of the mRNA for alpha 2u-globulin was examined with cultured hepatocytes derived from growth hormone-deficient rats. Culture of these cells in the presence of growth hormone for 24 h did not turn on the synthesis of alpha 2u-globulin. These results indicate that growth hormone regulates the synthesis of alpha 2u-globulin by acting at a step antecedent to mRNA translation.

Biochemical studies of some hydrolytic enzymes in malathion treated germinating seeds ofVigna sinensis(l): effect of growth hormone supplementation

Studies have been carried out on the different hydrolytic enzymes of the germinating seeds of V. sinensis (L) by exposing them to various concentrations of malathion (O, O dimethyl phosphorodithioate of diethyl mercaptosuccinate), an organophosphorus insecticide. At 50 ppm the insecticide induces the seedling growth and at 400 ppm caused a significant inhibition. On simultaneous application of either of the plant hormones, i.e., IAA, GA3 and kinetin with different concentrations of malathion, it was found that there was a trend to overcome of malathion inhibition of seedling growth. It was also found that treatment of seeds with growth hormones, at 400 ppm malathion exposure, helps to restore the normal activities of certain hydrolytic enzymes, which showed otherwise, significant altered activities. Kinetic studies show that the stimulation of acid phosphatase activity due to malathion exposure was non‐competitive in nature.

The effect of malathion on amino acid incorporation into plasma membrane proteins of Vigna sinensis (L): Effect of plant growth hormone supplementation.

Amino acid incorporation into plasma membrane proteins of Vigna sinensis (L) was inhibited by malathion, an organophosphorous insecticide, whereas some stimulatory effect was elicited by plant growth hormones, viz., IAA, GA3 and kinetin. The inhibitory effect of malathion towards amino acid incorporation into plasma membraneproteins was marked at concentrations above 50 ppm, and at 400 ppmthe amino acid incorporation was muchless. Up to 100 ppm of malathion treatment, the plant growth hormones could counteract the malathion-induced inhibition on amino acid incorporation into plasma membrane protein but above this concentration, the plant hormones gradually lost their effectiveness. Plasma membrane fraction was characterized by studying the activities of enzymes like IDPase, Oligomycin treated ATPase, Cytochrome ooxidase and glucan synthetase, and also by a sterol/phospho lipid ratio study. From the above studies it appears that glucan synthetase may be the marker enzyme of the plasma membrane of V. sinensis (L), and some change at the membrane level on malathion exposure is suggested.