Journal of Aquaculture Engineering and Fisheries Research

Characterization of functionalized multiwalled carbon nanotubes and comparison of their cellular toxicity between HEK 293 cells and zebra fish in vivo

Leandro Godoy^* Department of Animal Science, Federal University of Rio Grande do Sul, Brazil
^*Correspondence: Leandro Godoy, Department of Animal Science, Federal University of Rio Grande do Sul, Brazil, Email:

Received: Nov 01, 2022, Manuscript No. JAEFR-22-81161; Editor assigned: Nov 03, 2022, Pre QC No. JAEFR-22-81161 (PQ); Reviewed: Nov 17, 2022, QC No. JAEFR-22-81161; Revised: Nov 22, 2022, Manuscript No. JAEFR-22-81161 (R); Published: Nov 29, 2022, DOI: 10.3153/JAEFR.22.8.001

Citation: Leandro Godoy. Characterization of functionalized multiwalled carbon nanotubes and comparison of their cellular toxicity between HEK 293 cells and zebra fish in vivo. J Aquacult Eng Fish Res. 2022; 8(11)

Introduction

As a part of a large-scale chemical mutagenesis display of the zebra fish (Danio rerio) genome, we diagnosed 33 mutants faulty in hematopoiesis. Complement evaluation grouped 32 of those variations into 17 supplement groups. The final one blood mutant allele is presently unresolved [1]. These blood variations had been labeled into 4 phenotypic instructions with the aid of using in situ hybridization the use of the hematopoietic transcription elements GATA-1 and GATA- 2, primarily based totally on evaluation of entire embryos and remote blood cells. Embryos with mutated moonshine genes have few or no seen proerythroblasts at the day of access into circulation, blocked differentiation of everyday erythroid cells, as proven with the aid of using staining for hemoglobin, and shortage GATA-1 expression [2]. Mutations in 5 genes: Chablis, Frascati, Merlot, Retsina, and Thunderbird, and possibly particular mutations that cause a slow decline in blood counts at some point of the primary 5 days of improvement. Mutations in every other seven genes, Chardonnay, Chianti, Grenache, Sauternes, Weizenherbst, Zinfandel, and others, bring about hypochromic cells that lower in range as improvement progresses [3]. Some of those mutants have circulating immature cells, indicating that everyday erythroid improvement is disrupted. The Zinfandel mutation is dominant and 2-day-antique heterozygous vendors do now no longer specific detectable stages of hemoglobin and feature decreased circulating mobileular numbers at some point of the primary five days of improvement. Mutations in genes, Freixenet and Yquem, make animals with car fluorescent blood touchy to light, just like congenital porphyria in humans [4]. The series of mutants provided right here represents numerous steps required for everyday erythropoiesis. Analysis of those mutants offers an effective method to outline the molecular mechanisms worried in vertebrate hematopoietic improvement [5].

Description

Glycine mediates rapid inhibitory synaptic transmission. The physiological importance of glycinergic synapses is well established in the brainstem and spinal cord. In humans, loss of glycinergic function in the spinal cord and brainstem causes hypersensitivity characterized by exaggerated startle reflexes to sudden auditory or tactile stimuli [3]. It is also involved in motor regulation and nociceptive processing. The importance of glycinergic synapses is conserved across vertebrate species [1]. Zebra-fish, one of the teleost fish, offers several advantages as a vertebrate model for studying glycinergic synapses. A zebra-fish mutagenesis screen isolated two motility-deficient mutants with pathogenic mutations in glycinergic synaptic transmission: Bandoneon (beo) and Shock (sho) [4]. Beo mutants have loss-offunction mutations in the β subunit of the Glycine Receptor (GlyR). Alternatively, Sho mutants are defective glycinergic transporter 1 (GlyT1) mutants. These mutants are useful animal models for understanding glycinergic synaptic transmission and identifying new therapeutics for human diseases resulting from defects in glycinergic transmission, such as hypernephrosis and glycinic encephalopathy [2]. Recent advances in genome editing technology and imaging and manipulation of molecular or physiological processes have made the zebra-fish a more attractive model [5]. This review describes technical advances in both glycinergic deficient zebra-fish mutants, forward and reverses genetic approaches, and in vivo visualization and manipulation approaches to study glycinergic synapses in zebra-fish.

Conclusion

Histopathological evaluation of site-only, site-reversal, and site-ambiguous using zebra-fish models can advance research on heterotaxy. This study demonstrates that early visualization of cardiac loop defects can provide useful markers for selection of zebra-fish with lateral defects. It can be used for long-term studies or to study the histopathology of informative left-right visceral asymmetry. Research by reducing animals with a cross-layer background from model animals. In contrast, the development of a mutant zebra-fish model of FKRP by the TILLING process (targeting induced local lesions within the genome) using ENU-induced mutagenesis has been shown to affect skeletal muscle, the CNS, and the involved heart. These studies should help us understand the spectrum of phenotypes observed in human muscular dystrophies associated with mutations in the FKRP gene.

Acknowledgement

None.

Conflict of Interest

The author declares there is no conflict of interest in publishing this article.

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