Possible mechanism of bamboo shoots (Bambusa balcooa) induced thyroid disruption – An in vitro study. (March 2021)

• Record Type: Journal Article
• Authors: Sarkar, D; Chandra, AK; Chattopadyay, S; Biswas, M; Das, S; Singh, LH; Ray, I
• Is Part Of: Human & experimental toxicology. Volume 40:Number 3(2021)
• Page Start: 483
• Page End: 496
• Publication Date: 2021-03
• Subjects: Pendrin -- MCT8 -- thyroglobulin -- bamboo shoots -- thyrocytes -- cell cycle; Toxicology -- Periodicals; 615.9
• DOI: 10.1177/0960327120958037
• Languages: English
• ISSNs: 0960-3271

Abstract

Endemic goitre and associated iodine deficiency disorders (IDDs) are a major concern in public health even in the period of post salt iodization in many regions. Among others the consumption of cyanogenic plants found responsible for the persistence of such diseases. Bamboo shoots (BS) is one such cyanogenic plant food that caused disruption of certain thyroid hormone synthesizing regulatory element as has already been reported in our earlier study. In this investigation the possible mechanism of thyrocytes disruption along with interruption of thyroid hormone biosynthesis by BS has been worked out. Commonly consumed BS, Bambusa Balcooa Roxb (BBR) water extract was analysed by GC MS; three doses below IC50 were administered to thyrocytes in culture with and without iodine. Expressions of thyroglobulin (Tg), pendrin (PDS) and monocarboxylate transporter 8 (MCT8) were evaluated in thyrocytes with cell cycle analysis, reactive oxygen species (ROS) generation, DNA oxidation and apoptotic regulation through Bax, Bcl-2 and p53. Phytochemical analysis of BBR extract revealed the presence of precursors and metabolic end products of cyanogenic glycosides. Dose dependent decrease in expression of Tg and PDS with concomitant decrease in gene expression of these with MCT8 were observed. Increased ROS, DNA oxidation and associated imbalance were found through increased Bax and p53 with decreased Bcl-2 that perturbed thyrocytes cell cycle. Cyanogenic constituents of BBR generates ROS associated oxidative changes in thyrocytes with DNA damage and oxidation and cell cycle disruption followed by inhibition of thyroid hormone synthesizing regulatory elements; addition of extra iodine showed partial prevention.