Unpredictable chronic mild stress (UCMS) leads to variable metabolic effects. Oxidative stress (OS) of adipose tissue (AT) and mitochondrial energy homeostasis is little investigated. This work studied the effects of UCMS on OS and the antioxidant/redox status in AT and mitochondrial energy homeostasis in rats. Twenty‐four male Wistar rats (180–220 g) were divided into two equal groups; the normal control (NC) group and the UCMS group which were exposed to various stresses for 28 days. An indirect calorimetry machine was used to measure volumes of respiratory gases (VO2& VCO2), total energy expenditure (TEE), and food intake (FI). The AT depots were collected, weighed, and used for measuring activities and gene expression of key antioxidant enzymes (GPx1, SOD, CAT, GR, GCL, and GS), OS marker levels including superoxide anion (SA), peroxynitrite radical (PON), nitric oxide (NO), hydrogen peroxide (H2O2), lipid peroxides (LPO), t‐protein carbonyl content (PCC), and reduced/oxidized glutathione levels (GSH, GSSG). Additionally, AT mitochondrial fractions were used to determine the activities of the tricarboxylic acid cycle (TCA) cycle enzymes (CS, α‐KGDH, ICDH, SDH, MDH), respiratory chain complexes I–III, II–III, IV, the nicotinamide coenzymes NAD+, NADH, and ATP/ADP levels. Compared with the NC group, the UCMS group showed very significantly increased OS marker levels, lowered antioxidant enzyme activities and gene expression, as well as lowered TCA cycle and respiratory chain activity and NAD+, NADH, and ATP levels (p < .001 for all comparisons). Besides, the UCMS group had lowered TEE and insignificant FI and weight gain. In conclusion, AT of the UCMS‐subjected rats showed a state of disturbed redox balance linked to disrupted energy homeostasis producing augmentation of AT. Significance statement Adipose tissue (AT) during periods of unpredictable chronic mild stress (UCMS) may encounter some oxidative metabolic change. This work studied oxidative stress of AT and mitochondrial energy homeostasis in rats exposed to UCMS. This study detected profound oxidative stress (OS) in AT of UCMS‐subjected rats, leading to redox imbalance. Besides, the presence of a reduction of the tricarboxylic acid cycle (TCA) cycle and respiratory chain activities consequently marked reduction in adenosine triphosphate (ATP) levels, thus indicating mitochondrial metabolic exhaustion and disruption of energy homeostasis. These findings can impact the TEE and be associated parallelly with both TEE and food intake (FI), resulting in insignificant weight changes. Future research investigating the role of antioxidants as a prophylactic or curative treatment during UCMS is suggested.