New Complex of Cryptic Species Discovered in Genus Biblis (Papilionoidea: Nymphalidae: Biblidinae) in Mexico.

Our research focuses on demonstrating the existence of cryptic species named under Biblis aganisa Boisduval. We used COI sequences to delimit Biblis species for Mexico using species delimitation analyses and examined phylogenetic relationships with sequences from Mexico, Costa Rica, Argentina, USA, and Guana Island using a Bayesian inference tree. We performed a discriminant analysis with quantitative traits using female and male wing and genitalia, and a tree of maximum parsimony based on 39 qualitative characters of wings, head, and male genitalia. The results were congruent in the three analyses. Three groups were formed based on DNA, ECO 01 + DHJ02, ECO 02 + DHJ01, and ECO 03. The characters that contributed over 50% separation were for wings: wing length, anal margin length, and distance from the band to the outer margin; for male genitalia, angle of the integument, uncus, and the length of the hypandrium, while for females, it was the angle of the anteapophysis and the length of the abdomen. For the analysis of qualitative characters, a tree of maximum parsimony was obtained where 20 characters were informative. We confirmed the existence of three cryptic Biblis species in Mexico, two not yet described, and one corresponding to B. aganisa (ECO 02), which is sympatric in Oaxaca and Sinaloa (ECO 03) and in the Yucatan Peninsula (ECO 01).

Amino Acid Metabolomic Profiles in Bovine Mammary Epithelial Cells under Essential Amino Acid Restriction.

Mammary epithelial cells (MECs) in culture are a useful model for elucidating mammary gland metabolism and changes that occur under different nutrient disponibility. MECs were exposed to different treatments: 100% EAA for 8 h and 24 h restriction (R); 2% EAA for 8 h and 24 h R; 2% EAA for 8 h and 24 h + 100% EAA for 8 h and 24 h restriction + re-feeding (R + RF). Western blotting and protein quantification was performed. The Kyoto Encyclopedia of Genes and Genomes (KEGG) software identified the amino acids (AAs) and signaling pathways. The chi-squared test, multiple classification analysis, and analysis of variance were used for the purification and identification of data. Intracellular casein levels were not affected. The KEGG analysis revealed that the important pathways of metabolism of AAs, which were involved in processes related to metabolism and biosynthesis of phenylalanine, tyrosine, and tryptophan (fumarate, acetyl-CoA, and tricarboxylic acid (TCA) cycle), were affected by both R and R + RF treatments, mainly through the glutamic-oxaloacetic transaminase-2 enzyme. Additionally, metabolic processes mediated by the mitochondrial malate dehydrogenase, S-adenosylmethionine synthetase, and asparagine synthase proteins positively regulated the carbohydrate pathway, pyruvate, and TCA cycles, as well as the metabolism of alanine, aspartate, and glutamate metabolism (carbohydrate and TCA cycle). We hypothesized that MECs have the capacity to utilize alternative pathways that ensure the availability of substrates for composing milk proteins.

Metabolic responses in bullfrog, Lithobates catesbeianus after exposure to zinc, copper and cadmium.

This study investigated the activity of lactated dehydrogenase (LDH), malate dehydrogenase (MDH) enzymes and the levels of glucose, protein and triglyceride in bullfrog tadpoles after exposure to 1 µg L-1 of zinc (Zn), copper (Cu) and cadmium (Cd) isolated and combined for 2 and 16 days. Zn, Cu + Cd and Zn + Cu + Cd increased the activity of the LDH (2 and 16 days) and MDH (2 days) enzymes in the liver; and MDH increased in the kidney after 16 days in all co-exposed groups compared to the control. Glucose increased in the liver in the Zn and Cu groups at 2 and 16 days of exposure and decreased in the kidney (groups Cd, Zn + Cd and Cu + Cd) and muscle (Cd) at 2 days of exposure. After 2 days of exposure, the protein increased in the liver (Zn), in the kidney in all groups exposed to metals except in the groups exposed to Cd and Zn + Cu + Cd, which did not change and decreased in muscle in all the groups exposed to isolated metals. Regarding triglycerides, the kidney and muscle were the most affected, leading to a decrease in the Zn, Cu and Cd groups and in the Zn + Cu (16 days) and Zn + Cu + Cd groups (2 days). The anaerobiosis and aerobiosis were activated in the liver and kidney after short-term exposure (2 days) and in the kidney, the aerobic metabolism was activated after chronic exposure (16 days). The metals caused toxicity and were higher in co-exposure to metals with a potential to cause metabolism damage in L. catesbeianus.

α-Tocopherol administration blocks adaptive changes in cell NADH/NAD+ redox state and mitochondrial function leading to inhibition of gastric mucosa cell proliferation in rats.

In experimentally induced chronic gastritis, a compensatory mucosal cell proliferation occurs with enhanced glucose oxidative metabolism linked to lipoperoxidative events. Therefore, this study was aimed at assessing the participation of cell NAD/NADH redox state and mitochondrial functions during gastric mucosa proliferation and the effects of in vivo α-tocopherol (vitamin E) administration. Glucose oxidation and oxygen consumption were tested in gastric mucosa samples obtained from rats with gastritis and from those also treated with α-tocopherol. Gastric mucosal mitochondria were isolated and structural and functional parameters were determined. Succinate oxidation, ADP phosphorylation, mitochondrial enzyme activities, and membrane lipid composition were measured. In addition, parameters indicative of cellular NAD/NADH redox state, proliferation, apoptosis, and nitric oxide (NO) metabolism were also determined. After ethanol withdrawal, the damaged gastric mucosa increased glucose and oxygen consumption, events associated with a more reduced cytoplasmic NAD/NADH ratio. Enhanced mitochondrial oxidative phosphorylation and increased mitochondrial enzyme activities occurred early, accompanied by recovery of lost mitochondrial protein and lipid composition in the gastric mucosa, events associated with increased NO production. When mitochondrial function and structural events were normalized, apoptosis was initiated as assessed by the mitochondrial Bax/Bcl2 ratio. Treatment with α-tocopherol inhibited cell proliferation and blocked enhanced glucose utilization, mitochondrial substrate oxidation, and changes in redox state, delaying the onset of these adaptive metabolic changes, whereas it inhibited cell proliferation. In conclusion, α-tocopherol could abolish damage-induced "stress" signaling by desynchronizing mitochondrial adaptive responses, including mitochondria biogenesis, and consequently NAD/NADH redox, which seems to regulate gastric mucosal cell proliferation.