Oxidative stress is an imbalance between free radicals and the antioxidant system causing overgeneration of free radicals (oxygen‐containing molecules) ultimately leading to oxidative damage in terms of lipid peroxidation, protein denaturation, and DNA mutation. Oxidative stress can activate autophagy to alleviate oxidative damage and maintain normal physiological activities of cells by degrading damaged organelles or local cytoplasm. When oxidative stress is not eliminated by autophagy, it activates the apoptosis cascade. This review provides a brief summary of mitochondrial‐endoplasmic reticulum communication‐mediated oxidative stress and autophagy. Mitochondria and endoplasmic reticulum being important organelles in cells are directly or indirectly connected to each other through mitochondria‐associated endoplasmic reticulum membranes and jointly regulate oxidative stress and autophagy. The reactive oxygen species (ROS) produced by the mitochondrial respiratory chain are the main inducers of oxidative stress. Damaged mitochondria can be effectively cleared by the process of mitophagy mediated by PINK1/parkin pathway, Nix/BNIP3 pathways, and FUNDC1 pathway, avoiding excessive ROS production. However, the mechanism of mitochondrial‐endoplasmic reticulum communication in the regulation of oxidative stress and autophagy is rarely known. For this reason, this review explores the mutual connection of mitochondria and endoplasmic reticulum in mediating oxidative stress and autophagy through ROS and Ca²⁺ and aims to provide part of the theoretical basis for alleviating oxidative stress through autophagy mediated by mitochondrial‐endoplasmic reticulum communication.

Yaks living in the high-altitude hypoxic environment of Tibetan plateau (3600 m) have special gut microbes. However, it is still little research on yak probiotics until now. Therefore, the purpose of our study was to evaluate the growth promoting effect, antioxidant capability, immune effect, and anti-inflammatory ability of Bacillus subtilis and Bacillus velezensis isolated from Tibetan yaks in mice model. The results showed that the isolated strains supplementation not only improve the growth performance but also increased the length of villus in the small intestine and intestinal digestive enzyme activity. Importantly, we observed that the T-AOC, SOD, and GSH-PX levels were increased and the MDA content was reduced in probiotic-treated mice, which implied that probiotics supplementation can ameliorate the antioxidative activity of mice. The levels of AST and ALT correlated with the hepatic injury were reduced and the levels of AKP, TP, GLB, ALB, Ca, and P were markedly higher than those in the control group. Additionally, mice treated with probiotics exhibited higher serum IgG, IgM and IgA, which can reflect the immune status to some extent. At the same time, the major pro-inflammatory factor TNF-α, IL-6, and IL-8 were down-regulated and the anti-inflammatory factor IL-10 was up-regulated compared with the control groups. In conclusion, these results demonstrated that Bacillus subtilis and Bacillus velezensis supplementation can increase overall growth performance and ameliorate the blood parameters related to inflammation and immunity of mice.

Paraquat (PQ) is a cheap and an effective herbicide, which is widely being used worldwide to remove weeds in cultivated crop fields. However, it can cause soil and water pollution, and pose serious harm to the environment and organisms. Several countries have started to limit or prohibit the use of PQ because of the increasing number of human deaths. Its toxicity can damage the organisms with a multi-target mechanism, which has not been fully understood yet. That is why it is hard to treat as well. The current research on PQ focuses on its targeted organ, the lungs, in which PQ mostly trigger pulmonary fibrosis. While there is a lack of systematic research, there are few studies published discussing its toxic effects at systematic level. This review summarizes the major damages caused by PQ in different organisms and partial mechanisms by which it causes these damages. For this purpose, we consulted several research articles that studied the toxicity of PQ in various tissues. We also listed some drugs that can be used to alleviate the toxicity of PQ. However, at present, the effectiveness of these drugs is still being explored in animal experiments and the study of their mechanism will also help in understanding the poisoning mechanism of PQ, which will ultimately lead to effective treatment in future.