Enzymes In Offspring Research Articles

Transgenerational stress memory in plants is mediated by upregulation of the antioxidative system

Transgenerational stress memory transferred from parents to offspring may enable plants to respond to changing environments rapidly. Yet transgenerational adaptive effects and underlying mechanisms in response to waterlogging and drought are still unclear. Furthermore, transgenerational cross-stress tolerance, pre-adapting offspring to any stress when maternal plants experienced stress, is currently understudied. We conducted a full-factorial pot experiment over two generations, using four perennial plant species and subjecting maternal and offspring plants to waterlogging and drought. We hypothesized that offspring experiencing stress performed better when mothers had experienced stress before, irrespective of the type of stress. We found increased biomass and reproductive output in offspring experiencing the same stress conditions as their mothers (transgenerational adaptive effects). However, a maternal stress experience per se did not pre-condition offspring to other types of stress. Transgenerational adaptive effects were linked to changes in the antioxidative system of one species, reducing oxidative damage through upregulation of protective enzymes in offspring experiencing the same conditions as their mothers. Our research provides evidence for transgenerational waterlogging and drought memory and links this to underlying photosynthetic and redox-related mechanisms. Transgenerational adaptive effects acting on the antioxidative system might therefore contribute to the rapid responses of plants to environmental change.

Cadmium exposure during prenatal development causes progesterone disruptors in multiple generations via steroidogenic enzymes in rat ovarian granulosa cells.

Exposure to the heavy metal cadmium (Cd) in the environment is linked to adverse health. To fully understand the adverse effects of this important endocrine-disrupting compound (EDC) requires studies that address multigenerational effects and epigenetic mechanisms. The present study orally dosed pregnant SD rats with Cd from gestation day 1 until birth. First filial generation (F1) female rats were mated with untreated males to generate the secondary filial generation (F2). Ovarian granulosa cells (OGCs) were collected at postnatal day (PND) 56 from both generations after prenatal Cd exposure, and hormone secretion examinations showed a progesterone disorder. Significant decreases in steroidogenic enzymes (steroidogenic acute regulatory protein (StAR) and P450 cholesterol side-chain cleavage enzyme (CYP11A1)) were observed in F1 and F2 rats. However, F1 and F2 rats had different patterns of mRNA and protein expression of steroidogenic factor 1 (SF-1). We also found that microRNAs were significantly changed using a microarray, and miR-10b-5p and miR-27a-3p were upregulated in F1 and F2 rats. The COV434cell line microRNA-knockdown model showed that these two important microRNAs regulated the StAR-induced Cd effect on progesterone secretion. Overall, the results of this study indicate that prenatal Cd exposure causes cytotoxicity problems, progesterone disorder and microRNAs expression changed in a multigenerational manner. And progesterone disorder may interfere with the steroidogenic enzymes in offspring. The present study also revealed that environmental pollution produces multigenerational effects.

Prenatal metformin treatment in obese rats: Evaluation of liver norepinephrine and lipogenic enzymes in offspring

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Fructose intake during gestation and lactation differentially affects the expression of hippocampal neurosteroidogenic enzymes in rat offspring

ABSTRACTNeurosteroids, steroidal hormones synthesized de novo from cholesterol within the brain, stimulate hippocampal functions such as neuron protection and synapse formation. Previously, we examined the effect of maternal fructose on the transcriptional regulation of neurosteroidogenic enzymes. We found that the mRNA expression level of the steroidogenic acute regulatory protein (StAR), peripheral benzodiazepine receptor (PBR), cytochrome P450(11β), 11β-hydroxysteroid dehydrogenase (HSD), and 17β-HSD was altered. However, we could not determine whether maternal fructose intake played a role in the gestation or lactation period because the dam rats were fed fructose solution during both periods. Thus, in this study, we analyzed the hippocampi of the offspring of dams fed fructose during the gestation or lactation period. Maternal fructose consumption during either the gestation or lactation period did not affect the mRNA levels of StAR, P450(17α), 11β-HSD-2, and 17β-HSD-1. PBR expression was down-regulated, even when rats consumed fructose during the lactation period only, while fructose consumption during gestation tended to activate the expression of P450(11β)-2. We found that maternal fructose intake during gestation and lactation differentially affected the expression of hippocampal neurosteroidogenic enzymes in the offspring.

Maternal protein restriction affects gene expression and enzyme activity of intestinal disaccharidases in adult rat offspring.

This study investigated the consequences of intrauterine protein restriction on the gastrointestinal tract and particularly on the gene expression and activity of intestinal disaccharidases in the adult offspring. Wistar rat dams were fed isocaloric diets containing 6% protein (restricted, n = 8) or 17% protein (control, n = 8) throughout gestation. Male offspring (n = 5-8 in each group) were evaluated at 3 or 16 weeks of age. Maternal protein restriction during pregnancy produced offspring with growth restriction from birth (5.7 ± 0.1 vs 6.3 ± 0.1 g; mean ± SE) to weaning (42.4 ± 1.3 vs 49.1 ± 1.6 g), although at 16 weeks of age their body weight was similar to control (421.7 ± 8.9 and 428.5 ± 8.5 g). Maternal protein restriction also increased lactase activity in the proximal (0.23 ± 0.02 vs 0.15 ± 0.02), medial (0.30 ± 0.06 vs 0.14 ± 0.01) and distal (0.43 ± 0.07 vs 0.07 ± 0.02 U·g-1·min-1) small intestine, and mRNA lactase abundance in the proximal intestine (7.96 ± 1.11 vs 2.38 ± 0.47 relative units) of 3-week-old offspring rats. In addition, maternal protein restriction increased sucrase activity (1.20 ± 0.02 vs 0.91 ± 0.02 U·g-1·min-1) and sucrase mRNA abundance (4.48 ± 0.51 vs 1.95 ± 0.17 relative units) in the duodenum of 16-week-old rats. In conclusion, the present study shows for the first time that intrauterine protein restriction affects gene expression of intestinal enzymes in offspring.

Programming of hepatic insulin-sensitive enzymes in offspring of rat dams fed a protein-restricted diet.

Hepatic enzymes associated with glucose hemostasis were studied in offspring of dams fed either a 20% protein (control) or an isocaloric 8% protein (low-protein) diet during pregnancy and lactation. Additionally, offspring were exposed to maternal 8% protein diet only during gestation (recuperated) or lactation (postnatal low-protein). Glucokinase activity decreased (approximately 50%), whereas phosphoenolpyruvate carboxykinase (PEPCK) activity increased (approximately 100%), in the low-protein and recuperated offspring compared with controls (P < 0.001) at 21 days of age. However, the postnatal low-protein offspring had enzyme activities comparable with those of controls. These changes were still evident in 11-mo-old offspring weaned onto a normal laboratory chow. Parallel changes were apparent in mRNA levels of glucokinase and PEPCK in the low-protein male offspring. Thus the effect of programming metabolism extends not only to protein biochemistry but possibly also to the regulation of gene expression. Furthermore, these changes could not be attributed to glucagon or insulin, because ratios of these hormones were comparable between the control and low-protein groups.

Prenatal exposure to alcohol in rat: Effect on intestinal enzymes in offspring

Intestinal hydrolase activities were studied during postnatal development in the offspring of rats exposed to 20% ethanol during gestation; alcohol was withdrawn at birth. Controls received water during gestation. Sucrase, lactase, glucoamylase and aminopeptidase activities were determined 2 and 4 weeks after birth in the proximal jejunum. Offspring prenatally exposed to ethanol showed a deficit in body weight and lower aminopeptidase activity during the suckling period (2 weeks). These effects were reversible by 4 weeks when alcohol was withdrawn at birth. The prenatal exposure to ethanol did not change the pattern of sucrase maturation in the intestine of offsprings. The activities of lactase and glucoamylase were not modified following prenatal exposure to ethanol. In conclusion, exposure to ethanol during gestation caused decreased abilities for the intestine of the offspring to digest protein.

Development of rat liver and colon substrate cycle enzymes in offspring with and without prenatal exposure to a carcinogenic dose of 1,2-dimethylhydrazine

1. Pregnant F-344 rats were exposed by intubation to a single dose (35 mg/kg) of 1,2-dimethylhydrazine dihydrochloride or to an acetate buffer on day 14 of gestation. 2. A detailed examination of the effects of this dose of 1,2-dimethylhydrazine on brush border enzymes in the offspring was performed. 3. Changes in the liver and colon levels of the α-glycerophosphate and malate/aspartate substrate cycle enzymes were measured during the development; at days 17 and 20 of gestation and at 2, 6, 13, 20, 27, 55, 110 days and 1 year after birth. 4. It is concluded that metabolic energy enzymes, glutamate oxaloacetate transaminase and malate dehydrogenase, are more sensitive to 1,2-dimethylhydrazine treatment than are the brush border hydrolases or NAD- and Fp-linked α-glycerophosphate dehydrogenases.